November 25, 2024
6 min read
As promised, here is the fourth installment of the dry eye disease “Back to Basics” series requested by an audience member at a dinner presentation I gave last winter.
In part 1, we took a look at normal tears, of which we have three types: baseline, psychic and reflex. Part 2 was snuck into the annual September column on the state of anti-inflammatory treatment of dry eye disease (DED); nothing is more basic when you are treating DED than learning how to prescribe immunomodulators (a bit more of that to come here). Last month, I reviewed the basics when we are evaluating a patient for possible DED.
Which brings me to part 4, perhaps the final installment in the mini-epic: putting together the data from your basic examination to determine your initial treatment strategy. At the moment, I am sitting on the porch of my daughter and son-in-law’s home in the Low Country, 3 days away from hopping on a plane for Chicago and the American Academy of Ophthalmology meeting. Not gonna lie, I am a little bit distracted, although the “why” is a bit up in the air. Is it the 8-foot alligator in the pond just on the other side of the fence or the cacophony from my phone as it blows up with texts about Bausch + Lomb’s stock as Blackstone et al consider making a bid for the company?
Looks like an exciting convention coming up.
Your patient has had their initial visit. They took a survey that alerted you and your staff that DED was likely. If you used Ocular Surface Disease Index (OSDI), visual analog scale (VAS) or Standard Patient Evaluation of Eye Dryness (SPEED) evaluations, you have some sense of how poorly they are feeling. Using your trusty slit lamp, you examined their eyelids and eyelashes. You know if they have youthful lids or if everything has fallen victim to gravity. The presence of telangiectatic blood vessels has been noted, and you have identified and graded the presence of collarettes at the base of the eyelashes. No one, including you, has touched their lids, and no one has put anything in their eye yet, allowing you and your staff to test for corneal sensitivity and assess the tear film when it is close to its natural state.
Using a moistened fluorescein strip, you have colored the tear film so that you can evaluate the tear meniscus, count out tear breakup time and look for the presence of corneal and/or conjunctival staining. Your call on lissamine green; knock yourself out. You can put that in after you have evaluated the fluorescein and look at conjunctival staining. Are you going to do a Schirmer test? I do not think it matters if you push on the lids and evaluate the oil that is or is not expressed before or after putting in a topical anesthetic for a baseline tear production test.
So, what did you come up with, and how are you going to use that to choose your initial treatment?
Remember, this is a basics course. Treatment 101. We are only going to utilize stuff that is available to every eye doctor. First line, true therapeutics. With this in mind, job No. 1 is to decide if the primary driver of symptoms is aqueous deficiency (there is insufficient tear quantity) or evaporation (the tear quality is poor and does not lubricate the ocular surface adequately). Many of your patients will show evidence of both. After all, roughly 35% of DED patients have legitimate signs pointing either way.
Still, like standing at the front door for a first date, your first shot across the bow for each patient is as important as any other first impression. Too little treatment to bring early relief of their symptoms is like showing up for the prom in a Texas tuxedo with a corsage of dandelions. On the other hand, trying to treat every little thing you see on that first visit with multiple prescriptions and a three-page instruction list is just over the top. Like ringing the doorbell wearing a real tuxedo, a dozen red roses in hand and a chauffeured antique Rolls-Royce sitting at the curb to go see a drive-in movie.
Make this basics exercise easy: Your patient blinked like you stuck something in their eye. No neurotrophic keratitis. Look to make the diagnosis for the OG of DED first. Aqueous-deficient dry eye (ADDE) is simple and straightforward: There are not enough tears. The fluorescein-stained tear meniscus will be low. The tears covering the cornea will barely do the job. You will likely see obvious staining of both the cornea and the conjunctiva. This means inflammation. Treatment is geared toward increasing the amount of tears present and the duration of their presence while treating this inflammation.
As I pointed out in a summer blog post, best practices for this scenario have not budged since 2003. Prescribe an immunomodulator, lifitegrast or a cyclosporine. Yes, I know, there are meaningful differences between these molecules and between the various formulations of cyclosporine, and you may have a favorite option for a good reason. I surely do. But for this first prescription, make it easy: Prescribe the one that will remove the smallest number of dollars from the patient’s pocketbook. Now is not the time to pick a fight with either your patient or their insurance.
Make a good impression by giving them a short course of topical loteprednol or fluorometholone (price matters here, too) to make them feel better right away. Feel the urge to add artificial tears? I know, it is a tough habit to break. Branded, non-preserved hypotonic tears. When they come back to see you, reduce tear outflow by occluding their lower punctum in both eyes. We are big fans of Lacrifill (Nordic Pharma) for this. It is the only new thing in the ADDE world.
Convinced that evaporation is the primary cause of your patient’s symptoms? Probably a pretty good guess, with 50% pure evaporative dry eye (EDE) and 85% with at least some aspect of desiccation stress. The signature look for this is those angry telangiectasia on the lids, thick and goopy meibomian secretion if you can express any at all, and the biggie, a fast tear breakup time. Usually less than 5. Staining still means inflammation, and once again, you can make a better first impression with the gift of a 4-week pulse of topical steroids. No staining? Less is more; put a hold on those steroids. Basic blocking and tackling include daily lid heating (we like a microwave option like the classic Bruder mask) and high-quality omega-3 dietary supplementation.
Unlike ADDE, EDE has two truly revolutionary new treatments. If your patient has any sign of posterior blepharitis at all and you see more than two collarettes, you have just diagnosed Demodex blepharitis. Trust me, while this may not be the only cause of EDE, it is almost certainly a significant cause. Learn how to prescribe Xdemvy (lotilaner ophthalmic solution 0.25%, Tarsus Pharmaceuticals) utilizing a specialty pharmacy. January is right around the corner, and Medicare Part D will hopefully no longer be a barrier. Twice daily for 6 weeks and then stop. Alert patients that the Demodex will eventually return, and they will need to repeat treatment in the future.
Last, and most definitely not least, we now have a treatment that appears to directly reduce evaporation from the surface of the eye, reducing both the symptoms and the signs of DED. Miebo (perfluorohexyloctane ophthalmic solution, Bausch + Lomb) is a fluorinated alkane that produces a molecular monolayer on the surface of the eye. Depending on how you measure it, more than 50% of Miebo remains on the ocular surface 6 hours after instillation. Phase 3 study subjects had an average decrease in DED symptoms of nearly 40%. If memory serves (remember, I am keeping one eye on an 8-foot alligator), corneal staining was decreased as early as 4 weeks after initiating treatment. Both symptoms and signs continued to be improved after 3 months and 6 months. Pro tip: no artificial tear use with Miebo. Leave that monolayer alone.
There you have it. Making the diagnosis utilizing stuff everyone has in their office. How to choose your first treatment regimen by making a best hypothesis about the primary type of DED causing your patient’s discomfort. A simple protocol available to any eye doctor designed to maximize the likelihood that you will make a good first impression by making patients feel better, hopefully without the need to take out a second mortgage. This is about as basic as it gets, and honestly, you can do an awful lot of good for an awfully large bunch of folks who are really suffering.
And with that I am off to Chicago and the annual AAO convention. I am on pins and needles to watch Brent Saunders, you know, Brenting. If you saw me, I sure hope you came up and said hello.
- For more information:
- Darrell E. White, MD, of SkyVision Centers in Westlake, Ohio, can be reached at dwhite@healio.com.
Sources/Disclosures
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Expert Submission
Disclosures:
White reports speaking and consulting for Allergan, Bausch + Lomb, Sun, Tarsus and Viatris, consulting for Aldeyra, Bruder, Nordic Pharma and Thea, and consulting for and being an investor in Orasis.
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