Not a day goes by without a patient telling me that they have dry eye. I am sure it’s the same for many of you. However, in my practice, most patients are surprised when I tell them they don’t actually have dry eye, just tears that aren’t working properly. Most of these “dry eye” sufferers make plenty of tears.

A big reason for the continuing confusion among “dry eye” patients is frankly, us. Most clinicians were taught, and many of us still firmly believe, that dryness is due to a lack of tears. This despite the clinical enlightenment of the last decade that established the key role of meibomian gland dysfunction in what we persist in wrongly describing as dry eye.

Even the well-informed amongst us have got it mostly wrong. We are so brainwashed on dry eyes being dry that we have a need to attribute “dry eye” to either tear evaporation or a lack of aqueous production. While these both usually play some role, it is actually the loss of tear stability, surface protection and failure of the homeostatic mechanisms that serve to right the listing “dry eye” ship that cause most of the signs and symptoms that we and our patients attribute to dry eye.

So, what about the patient with Sjogren’s or rheumatoid arthritis, you ask? Yes, most do have diminished tear production, but tell me how you fix this? By adding artificial tears or plugging their puncta? Good luck with that. In my experience, treating co-morbid MGD does more to address the signs and symptoms of these patients than even the best artificial tears will. A lipid-deficient tear film loses aqueous through evaporation and is inherently unstable, while an aqueous-deficient tear film, even in the rare circumstance of adequate and normal lipid levels, also becomes rapidly unstable and unprotective. In the overwhelming majority of “dry eye” patients, neither aqueous deficient nor evaporative issues exist in isolation; rather, they exist on an interrelated continuum of dysfunction, each interacting with and influencing the other.

By reducing dry eye to a discussion of tears and tear volume, we ignore the multitude of centrally and locally controlled homeostatic mechanisms that adjust myriad elements that stabilize and preserve tear structure and function, and provide ocular surface protection. Perhaps more importantly, today’s clinical reality is that we have more ways of effectively addressing insufficient lipid than insufficient aqueous. Thankfully, treating meibomian gland dysfunction is surprisingly effective in restoring tear stability and function, and improving patient symptoms—even in patients who are aqueous deficient.

It’s time we let go of the antiquated dry eye model and better understand the exquisite complexity of the ocular surface environment. The sooner we do that, the better for our patients.

Arthur B. Epstein, OD, FAAO Chief Medical Editor artepstein@optometricphysician.com