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Intervening early in dry eye disease: reducing patient cost and disease burden

Optometry 360

By Mila Ioussifova, OD, FAAO

The contents of this article are informational only and are not intended to be a substitute for professional medical advice, diagnosis, or treatment recommendations. This editorial presents the views and experiences of the author and does not reflect the opinions or recommendations of the publisher of Optometry 360.

Dry eye disease (DED) can place a tremendous burden on patients’ pocketbooks and quality of life.1 My practice is heavily focused on DED, and many of my patients come to me as referrals after seeing multiple doctors and paying for numerous treatments without experiencing relief. In addition to copays and the cost of the treatments themselves, these patients have often had to limit their working hours due to the discomfort of DED, reducing their earning power even as their healthcare costs are increasing. In some really severe cases, I have had patients whose DED has forced them to forego work entirely and rely on disability.

Beyond just work, DED often forces these patients to modify their lifestyle and stops them from enjoying many of the activities that they hold dear. The impact of this can be hard to understand until you actually start treating these patients and see firsthand the toll this takes; one study even found that patients with highly symptomatic DED experienced health-related quality of life decreases greater than those with macular degeneration that causes visual impairment.1

By screening for DED early and intervening as soon as possible, we can go a long way toward helping these patients, which starts with obtaining an early understanding of the root causes driving an individual’s disease.

Screening for and Diagnosing DED

One of the challenges with DED is that many patients present with nonspecific symptoms, like itchy eyes, fluctuating vision, and contact lens intolerance.2 Often, these patients don’t know that DED is what is driving their discomfort and will think it’s their contact lens prescription or glasses that need to be updated. Even worse, sometimes they confuse their itchy and watery eyes with allergies and self-treat with antihistamines, which can possibly exacerbate DED.3 Unfortunately, the vagueness of these symptoms can often lead to diagnostic delays, during which the disease progresses.

In reality, DED is not just 1 disease but an umbrella term that contains a wide variety of conditions that disrupt the homeostasis of the ocular surface4; the goal of screening should be to identify the underlying dysfunction that is driving loss of homeostasis in that individual. Because of this, and because there is a classic disconnect between signs and symptoms in DED,5 it is vital to always screen patients for DED in a comprehensive manner. This means not just looking through a slit lamp but also doing gland imaging, testing gland expressibility, and performing corneal fluorescein staining. Having a detailed discussion with your patient to understand what lifestyle or environmental factors could be driving their disease is also key.

Corneal sensitivity testing is another integral part of screening for DED. As DED progresses, the corneal nerves become damaged, reducing sensitivity; because these nerves contribute to ocular surface homeostasis, their damage can perpetuate the “vicious cycle” of DED progression.6 In fact, the results of 1 study indicate that as many as 30% of patients with DED have reduced corneal sensitivity.7 As such, I always perform corneal sensitivity testing when patients first present to my clinic so we can begin intervention as soon as possible for those who need it.

 Intervening Early With an Etiological Approach

When coming up with a treatment plan for patients with DED, I consider all factors contributing to their loss of ocular surface homeostasis. For patients with evaporative disease, I try to address meibomian gland dysfunction with a combination of in-office procedures like intense pulsed light or LipiFlow® (Johnson & Johnson) and drops like perfluorohexyloctane that can help reduce evaporation. For patients with aqueous-deficient disease, I confront the inflammatory component as well as increase tear production; cyclosporine can be useful here, as can neuromodulators like acoltremon or varenicline.4

In any patient who has shown reduced corneal sensitivity or whose epithelium is not healing as it should, I introduce cryopreserved amniotic membrane (CAM) therapy as quickly as possible. Because of its anti-inflammatory, anti-scarring, and antiangiogenic properties,8 CAM can quickly reduce inflammation and help jumpstart the healing process, with benefits beginning just a few days after placement and lasting for up to 4 months following a single treatment.9 As many treatments for DED take months to show efficacy, this quick relief can be life-changing for patients, and in my personal experience, it also helps enhance the efficacy of other concomitant treatments.

For these patients, I have typically used Prokera® Slim (BioTissue, Inc), but a new shelf-stable, ringless formulation has become available (CAM360 Amniograft™; BioTissue, Inc.), which may be more comfortable for patients and more convenient for providers since it does not require dedicated freezer storage. When applying the CAM, I combine it with a collagen shield, a partial tarsorrhaphy, and in-office antibiotic drops, and I also provide the patient with preservative-free artificial tears to use at home. Another approach is to use a bandage contact lens instead of a collagen shield, but I have personally experienced better results with the collagen shield.

Unlike many other in-office procedures, CAM therapies for ocular surface disease are billable to insurance, which can be a boon for cost-conscious patients, especially Medicare patients who may have already spent a large amount on their eye care and may be financially constrained.

Conclusions

Because of its wide prevalence and the disconnect between symptoms and signs, we should be checking for DED in most, if not all, patients. By doing comprehensive assessments that integrate corneal staining and sensitivity, we can begin intervention early and save these patients from potentially ending up with a much more complicated and difficult-to-manage disease that could exact costs on both their ocular health and wallet.

Mila Ioussifova, OD, CNS, FAAO, FOWNS, is the owner of South Waterfront Eye Care in Portland, OR, where she has practiced for the last 12 years. Dr. Ioussifova has a special interest in both ocular nutrition and preventative care and is involved in clinical education, didactics, and the training of future optometrists. Disclosures: She is a consultant for AbbVie, BioTissue, BlephEx, Brill, Harrow, Johnson & Johnson, Lumenis, NuVissa, Optase, Reichert, and Tarsus, as well as a speaker for Alcon, Bausch + Lomb, BioTissue, Dompe, Johnson & Johnson, Sight Sciences, and Sun Pharma.

References

  1. Morthen MK, Magno MS, Utheim TP, Snieder H, Hammond CJ, Vehof J. The physical and mental burden of dry eye disease: a large population-based study investigating the relationship with health-related quality of life and its determinants. Ocul Surf. 2021;21:107-117. doi:10.1016/j.jtos.2021.05.006
  2. Guo OD LW, Akpek E. The negative effects of dry eye disease on quality of life and visual function. Turk J Med Sci. 2020;50(SI-2):1611-1615. doi:10.3906/sag-2002-143
  3. Britten-Jones AC, Wang MTM, Samuels I, Jennings C, Stapleton F, Craig JP. Epidemiology and risk factors of dry eye disease: considerations for clinical management. Medicina (Kaunas). 2024;60(9):1458. doi:10.3390/medicina60091458
  4. Jones L, Craig JP, Markoulli M, et al. TFOS DEWS III: management and therapy. Am J Ophthalmol. 2025;279:289-386. doi:10.1016/j.ajo.2025.05.039
  5. 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
  6. Vereertbrugghen A, Galletti JG. Corneal nerves and their role in dry eye pathophysiology. Exp Eye Res. 2022;222:109191. doi:10.1016/j.exer.2022.109191
  7. Stolz M. The prevalence of corneal sensitivity loss in patients with and without dry eye disease. Clin Ophthalmol. 2025;19:1323-1330. doi:10.2147/OPTH.S513005
  8. Zhang Y, Helman A, Mead OG, Tighe S, Zhu Y, Tseng SCG. Processing methods affect biological properties of amniotic membrane sheet products. Cornea. 2025;44(6):671-678. doi:10.1097/ICO.0000000000003849
  9. 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

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