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Guest Editorial

A witness to 14 years of relentless progress

Ophthalmology never just accepts the status quo.

If a single word describes ophthalmology as a field, “dynamic” comes first to my mind. The constant I have noticed, after 14 years in this specialty, is that its people, whether working in industry, academia or medical practice, generally have an unstoppable drive to push beyond the status quo. Progress is the norm — in techniques, technologies, efficiencies.

I’m well aware that we all face hurdles of declining reimbursements and its potential detriment to quality of work, but I feel blessed that ophthalmology is not stagnant intellectually. This is especially true in the subspecialties of ocular surface disease (OSD) management and refractive surgery.

In the realm of OSD, two recently published studies — CEDARS dysfunctional tear syndrome treatment strategies and the TFOS DEWS II report — serve as testament to how much OSD has evolved, from diagnostic methodologies to newer treatment options to a better understanding of how masqueraders and dysfunctional hyperaesthetic corneal pain affect OSD. The days of artificial tears, warm washcloth compresses and baby shampoo considered the only dry-eye therapies — as was the case in 2004, when I was a resident — are long gone. Today, I routinely consider a three-pronged approach: topical anti-inflammatory; intervention to maximize the ocular surface architecture (meibomian glands, conjunctival redundancy); and systemic therapy (i.e., oral omegas, limiting oral medications such as anti-histamines if possible).

As a refractive and cataract surgeon in 2018, I know that identifying OSD is ever more important, to the point that meibography is part of all my surgical evaluations. Meibography has taught me two important lessons. First, meibomian gland disease (MGD) can be seen in extremely young patients; this is a distressing reality because of the implications of more severe OSD in years to come. Second, many people have healthier meibomian gland architecture on meibography than I anticipated. At one time, ophthalmologists thought poor quality (thick, hard to express) meibum came from “bad glands,” or bad architecture. It turns out that poor meibum, a product of MGD, often comes out of healthier appearing glands. This is relevant in two ways: 1. In those with good architecture, MGD responds more favorably to thermal/thermal pulsation therapy (because the architecture is still healthy, and many glands still will produce oil), and; 2. MGD occurs first, then leads to damage ... not the other way around.

Regarding refractive surgery innovations, we have entered the era of corneal inlays. While this therapy has had its starts and fits from a few vantage points, we finally have a viable nonexcimer laser-based form of corneal presbyopia correction.

And last, I loved seeing that more than one-third of presentations at ASCRS’s Annual Meeting Refractive Day last month were devoted to lens-based refractive surgery options; refractive surgery no longer implies “corneal.” OM