Simplifying the treatment of ocular surface disease

Ocular surface disease (OSD) is one of the most challenging yet rewarding conditions to treat. In my practice, which is embedded within a multispecialty ophthalmology setting, I typically see 35 patients with OSD each day, most of whom have already seen multiple providers. As we serve a large population of older patients who are often undergoing cataract surgery, glaucoma management, or retina care, we routinely encounter patients whose OSD is either contributing to or being worsened by their underlying ophthalmic comorbidities. Many of these patients require chronic therapy, long-term monitoring, and ongoing rehabilitation. As such, successfully treating them requires advanced knowledge of each condition and of how they interact when they coexist.

Understanding the complexity of OSD

When clinicians think about OSD, they usually think of dry eye. However, dry eye is an umbrella term that encompasses multiple subtypes and overlapping mechanisms.¹ It is possible for patients to concomitantly have evaporative dry eye, inflammatory dry eye, meibomian gland dysfunction, corneal nerve abnormalities, exposure-related disease, and medication toxicity.

Another challenge is that some patients present with severe symptoms despite minimal clinical findings, whereas others exhibit significant corneal disease with surprisingly little discomfort. This disconnect between signs and symptoms can easily lead to misdiagnosis or undertreatment if clinicians rely solely on a slit lamp observation to make their diagnosis.² This problem is especially salient for patients with neurotrophic disease, as historically many of these patients were not diagnosed until the disease had already significantly progressed. Now there is a growing emphasis on earlier corneal sensitivity testing for all patients with OSD to allow for earlier intervention.

We must also acknowledge the role that chronic medication usage plays in OSD. For example, my patients with glaucoma may develop significant ocular surface toxicity from the preservatives in their medications. Ironically, they are often more bothered by the adverse effects of these medications than by the glaucoma itself. Patient adherence plummets when they experience burning, tearing, photophobia, or chronic discomfort, and we need to ensure we are not creating a new problem while treating another.³

Taking a holistic approach to OSD management

One of the biggest misconceptions in OSD management is the idea that a single drop or procedure can resolve every problem; successful management requires addressing the entire ocular surface ecosystem, beginning with the lids and lashes.

In our practice, we routinely incorporate meibography and evaluate blink dynamics, meibomian gland function, lid laxity, and any other evaporative contributors. Blink dysfunction and lid laxity in particular can significantly affect corneal health, contributing to corneal nerve abnormalities and even neurotrophic disease. When clinically appropriate, we utilize therapies such as intense pulsed light, radiofrequency, and dynamic muscle stimulation to help address these issues.

Treating OSD: From inflammation to nerve regeneration

As inflammation is the hallmark of OSD, much of our treatment strategy centers around targeting and suppressing the inflammatory burden.⁴ When we think about inflammation on the ocular surface, it is important to think beyond just the lids and conjunctiva. The cornea is central to visual function, and corneal consequences directly affect visual quality and patient satisfaction. Cequa (cyclosporine ophthalmic solution 0.09%; Sun Pharmaceutical Industries) and Xiidra (lifitegrast ophthalmic solution 5%; Bausch + Lomb) are valuable long-term tools, and corticosteroids continue to serve as effective induction therapies or flare-management options.⁴ Therapies that do not directly target inflammation can also be useful; neuromodulators like Tryptyr (acoltremon ophthalmic solution 0.003%; Alcon), for example, can increase natural tear production in aqueous-deficient patients,⁵ and antievaporative agents like Miebo (perfluorohexyloctane ophthalmic solution; Bausch + Lomb) can help stabilize the tear film in patients with evaporative dry eye.⁶

One of the most important changes in OSD management has been the shift from maintenance to true rehabilitation, with therapies that can help restore ocular surface health. In my practice, we have done this for more than a decade with cryopreserved amniotic membrane (CAM) therapies, which provide anti-inflammatory, antiscarring, and antiangiogenic benefits to the ocular surface. Traditionally, I have used the self-retained formulation of CAM (Prokera, BioTissue), but the recent introduction of a ringless, shelf-stable option (CAM360 AmnioGraft; CAM360 AG; BioTissue) has helped expand access to this therapy, as it requires no dedicated freezer storage.⁷

When using CAM360 AG, I routinely pair it with a collagen shield and a partial tape tarsorrhaphy. The efficacy of this approach was highlighted in a recent, single-center, retrospective study, where the combination of CAM360 with a collagen shield or bandage contact lens (BCL) and partial tape tarsorrhaphy resulted in significant improvements in signs and symptoms of OSD within 96 hours, with benefits lasting up to 4 months.⁷ I prefer the collagen shield to the BCL for this approach; in my experience, the use of a BCL frequently requires prophylactic antibiotic coverage and more intensive follow-up. If bilateral treatment is necessary, I often treat one eye initially and bring the patient back several days later to address the fellow eye.

Throughout CAM360 AG treatment, I usually instruct patients to use preservative-free artificial tears 4 times daily and to stop lubricating the eye at day 3; as lubrication decreases, the collagen shield and CAM360 AG naturally dissolve without requiring an in-office removal appointment.⁸ This has significant implications for both patient convenience and practice efficiency; in a busy referral-based practice like mine, where many patients travel long distances for care, eliminating unnecessary follow-up visits reduces patient and clinic burden while helping preserve clinical flow.

Conclusion

There is no universal protocol for managing OSD. Instead, successful OSD management comes from paying attention to the details. It’s important not only to understand the specific mechanisms driving an individual’s disease, but also to discuss with patients their visual goals, the adverse effects they can and can’t tolerate, and what matters most to them in their treatment journey. With a thoughtful approach and the right therapies, we can give patients with this chronic, progressive, and often frustrating disease new opportunities for restored corneal health, clearer vision, and improved quality of life.

References:

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2. Bartlett JD, Keith MS, Sudharshan L, Snedecor SJ. Associations between signs and symptoms of dry eye disease: a systematic review. Clin Ophthalmol. 2015;9:1719-1730. doi:10.2147/OPTH.S89700

3. Rosin LM, Bell NP. Preservative toxicity in glaucoma medication: clinical evaluation of benzalkonium chloride-free 0.5% timolol eye drops. Clin Ophthalmol. 2013;7:2131-2135. doi:10.2147/OPTH.S41358

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7. Cushman S. Shelf-stable, cryopreserved amniotic membrane for the management of ocular surface disease: a retrospective assessment. Clin Optom (Auckl). 2025;17:409-415. doi:10.2147/OPTO.S563708

8. Rana D, Desai N, Salave S, et al. Collagen-based hydrogels for the eye: a comprehensive review. Gels. 2023;9(8):643. doi:10.3390/gels9080643