In part 2 of a 5-part video series, Marjan Farid, MD, of the University of California, Irvine; Karolinne Rocha, MD, PhD, of the Medical University of South Carolina; Nathan Lighthizer, OD, of the Northeastern State University Oklahoma College of Optometry; and Cory Lappin, OD, the Dry Center of Ohio, discuss the dry eye cycle and the role of improving the patient’s own natural tears as part of treatment.
Marjan Farid, MD:
Karolinne, I’m going to ask you. We’ve had traditionally the therapeutics that were approved early on were related to tear film inflammation really, and certainly inflammation plays a role in dry eye disease. But does it start with inflammation? Is inflammation at the beginning or is there loss of homeostasis and tear dysfunction earlier on?
Where do you start with therapeutics? We have so many things. Where do you jump to? Do you to the anti-inflammatory? Do you start with something else? There are some really excellent things out there now. Tell me about your algorithm.
Karolinne Rocha, MD, PhD:
Sure. Thank you, Marjan. This is a great question and I really agree with you. It is so important to tell the patients this is a chronic disease, right? That follow-up is really important. We talking about the disease that affects 38 million people in United States.
Patients, they come in sometimes just complaining of blurry vision. You check the vision, 20/20 vision and it’s dry eye disease, right, with all the other symptoms that we see—discomfort, hyperemia, light sensitivity, tearing, sometimes even mucus. It can be very debilitating.
I think I like to approach, I’d say all the different phases of dry eye disease. We see that young patient with the computer syndrome, the computer all day long. You mentioned the contact lens wear and then, of course, in the cornea clinic we’ll see neurotrophic corneas and patients with autoimmune diseases.
But I think, Marjan, I really like your question because it’s important to go back a little bit in that dry eye cycle, right, to understand a little bit. We initially see hyperosmolarity with tear film instability and that will basically activate events in the surface of epithelial cells.
Then it’s when we start seeing the release of inflammatory mediators or the cytokines, right? It’s when that starts affecting the goblet cells. We start seeing the epithelial cell walls and damage and then again, all these inflammatory mediators and we see activated T cells in the ocular surface.
With all that going on is when that patient comes in with the PE, right, the punctate erosions and tear film instability and the break up time, it’s abnormal. But I think, again, when I see a patient, I always want to look at the big buckets of dry eye disease, tear film instability.
Very important to look at the lids, MGD, blepharitis, right? You can assess tear film production, you can assess osmolarity. In our clinics, also quality of vision, right? Some devices that can help us now to look actually to show us how the patients are seeing because of the tear film instability.
Then in terms of treatment, right, so you can use drops and things that can reduce inflammation or maybe increase the tear film production and you can target tear film stability. Of course you want to always treat the eyelid margin disease.
Marjan Farid, MD:
Absolutely. It’s very interesting because if you look upstream, it does start with hyperosmolarity and that’s when you have basically an imbalance of the tear components, right? The mucin layer and you get dehydration of the tear film and so that increases the osmolarity of the entire tear film.
I think, really, if we want to start upstream, there is a role for normalizing the normal tear film before it continues down this stream and becomes inflammatory. I think there’s really a role of improving the patient’s own natural tears.
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