Laura Periman, MD, founder and director of Dry Eye Services and Clinical Research in Seattle, spoke with Ophthalmology 360 at the American Society of Cataract and Refractive Surgery Annual Meeting on the topic of optimal dry eye disease management.
Laura Periman, MD:
I want to talk to you about a clinical situation that we’re starting to learn a lot more about, and that is saponification on the lid margin. What creates that? Well, it turns out lipases are the enzyme that break down host lipids into free fatty acids, and that’s what you’ll see as saponification on the lid margin. Here’s what I’ve come to learn and I want to share with you. Saponification from lipases can come from a variety of organisms, staph, strep, Bacillus species, and some Carinii bacterium, some pseudomonas. In the case of pseudomonas, that’s one of the strategies they use to break down the host barrier to create disruptions in the corneal epithelial barrier function and establish infection.
But I’m talking about lid margin disease for the moment. When you go back and look 60 seconds after your diagnostic or therapeutic meibomian gland expression, look for foam cells saponification on the lid margin. That doesn’t show up for about 60 seconds after you do that part of your exam. Go back and look just very briefly and it can indicate a variety of problems on the ocular surface.
Number one, Demodex. Demodex folliculorum, Demodex brevis, they have a gut organism that’s in the bacillus family. It’s called Bacillus oleronius, and this is a possible source of some of these lipases. My clinical strategy is to do 2 courses of topical lotilaner ophthalmic solution twice a day for 2 full courses of therapy. The poster we had for ASCRS is a case of dramatically improved foam cells or saponification on the lid margin with 2 courses of therapy, implying that Demodex brevis is a component and may need a longer course of therapy.
Number 2 is an uncommonly identified and treated component to lid margin disease, and I’m talking about seborrhea. Seborrhea, as you recall, is from a fungal organism called Malassezia furfur. If you remember back to your histology days in medical school, it looks like spaghetti and meatballs under the microscope. This organism, its strategy for nutritional survival is to secrete lipases, lipases that break down the host fats into free fatty acids that it then absorbs for nutrition.
When you’ve cleaned up the rosacea, you’ve cleaned up the Demodex and you still have saponification, think about fungal organisms such as Malassezia furfur. My clinical strategy is topical ketoconazole, 2% shampoo twice a week, ketoconazole cream to the face every night after the face is clean. In severe cases, I’m using oral itraconazole, it’s BID with food for 10 days, followed by BID for 2 days for the first 2 days of the following 2 months. For example, if you finish that course of therapy on April 30, that 10-day course, you would do two days, May 30 and June 30. We’re seeing dramatic reduction in the saponification.
Other strategies that we’re using is a direct plasma pen treatment to the back side of the eyelids with either jet plasma pen or the NuVissa Plasma Pen. As we get good at identifying all these components to dry eye disease, that vexing multifactorial problem, we’re starting to get clarity about what to do when. Go ahead and pick off the easy fruit first. Treat the Demodex, get the rosacea under control. But don’t forget about other things such as seborrhea in your dry disease patients, and you’ll find even better clinical results taking this multidisciplinary approach in stride.
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