Treating dry eye 301: Advanced treatment strategies
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In our pandemic era in which all things educational have been turned upside down, we here at The Dry Eye have produced a series that is perfect for study in the comfort of your bath, er, living room.
Beginning with “Treating dry eye 101,” we reviewed the various ways that we diagnose and characterize the various types of DED. In “Treating dry eye 201,” we took our fine-tuned diagnosis and utilized the data generated in the history and exam to tailor a “first shot across the bow” treatment for a new DED patient. Today we introduce advanced treatment strategies in our 301 course.
A super-majority of patients with DED will be adequately treated with an immunomodulator (Restasis/Cequa/Xiidra) and an artificial tear chosen to match the DED subtype (aqueous deficient vs. evaporative). Patients who are found to have low tear volumes on Schirmer testing will benefit from the placement of punctal plugs once ocular surface inflammation is brought under control. Controlling the inflammation may require a short course of adjuvant topical steroid use during the immunomodulator induction period; for this, our clinic typically uses Flarex (Eyevance Pharmaceuticals) because of the strength of the acetate version of fluorometholone. When your otherwise stable patient suffers an inevitable DED flare, the easiest way to handle that is with a newer topical steroid, Eysuvis (loteprednol etabonate ophthalmic suspension 0.25%, Kala Pharmaceuticals), which is FDA approved for this specific indication.
While you will undoubtedly make most of your patients comfortable and improve their ability to perform their daily activities without DED-related limitations, we all know there will be patients who will require more. In general, this means addressing one of three problems: incompletely treated surface inflammation, ongoing meibomian gland dysfunction (MGD) and conjunctivochalasis (CC). Let us begin with inflammation.
Symptomatic inflammation despite fully implemented immunomodulator treatment is the most common cause of what Mark Milner calls “false failures.” If you look carefully at the arc of these patients’ history, paying close attention to their DED questionnaire, you will inevitably find that their symptoms have improved over the course of their treatment, sometimes dramatically so. The fact that they are not completely asymptomatic, or that you still see or measure some ocular surface inflammation or other abnormality, does not mean that your course of action has failed. Similar to glaucoma care in which a 25% decrease in IOP does not get you all the way to your pressure goal, your initial 25% IOP improvement was hardly a failure; you just need additional treatment.
Traditionally, one would add a topical steroid here and call it a day. I usually anticipate that this will be a long-term proposition and accordingly prescribe whichever loteprednol formulation will be best covered by insurance. These patients need to be seen every 3 months for a pressure check. Maddeningly, just like all of those mutual fund commercial disclaimers that past performance does not predict future outcomes, the fact that your long-term steroid patient has not had an IOP rise in 2 years does not mean they will not have one over the more convenient 6-month interval you would rather they be on. Once upon a time, we would handle this by using both cyclosporine A and lifitegrast at the same time. Due to the universal rejection of this strategy by every health insurance company in America, this is no longer realistic.
Patients with CC who have completely treated inflammation but continue to have bothersome symptoms need to be addressed surgically. Period. You can futz around with different artificial tears, maybe encourage them to use Lumify (brimonidine tartrate ophthalmic solution 0.025%, Bausch + Lomb) to reduce redness, but in the end, there is no medical therapy that will solve the problem of stretched-out, floppy conjunctiva (insert your own bad liposuction joke here). You do have options, though. Rolando Toyos (classic heat) and Steve Safran (radiofrequency) have YouTube videos demonstrating their versions of cautery performed on forniceal conjunctiva to stretch and tighten the interpalpebral tissue. Both are relatively quick and painless. Both Drs. Toyos and Safran report positive patient responses.
Alternatively, you can excise the redundant conjunctiva, utilizing an amniotic membrane graft to promote healing over the surgically created defect. Again, there are two variations of this theme, both also available to view on YouTube. John Hovanesian describes an approach in which he resects the offending conjunctiva at the limbus, while Neel Desai prefers to shorten the conjunctiva by doing a resection in the inferior fornix. The use of amniotic membrane grafts promotes a quieter recovery with less chance of scarring. Both approaches require some dexterity and a bit of speed; tissue glue seals in less than 30 seconds whether or not you are done.
Finally, the big bugaboo when treating inflammatory DED is somehow improving the health of the meibomian glands, resulting in more, and better, oil in the tears. You can make your “go/no-go” call on using advanced MGD treatments based solely on what you see at the slit lamp (quick tear breakup time, telangiectasia, abnormal expression, etc), but like so many other things in life, “seeing is believing.” Imaging the meibomian glands with LipiView/LipiScan (Johnson & Johnson Vision), Meibox (Box Medical Solutions) or any of the other instruments available will show you, the doctor, the degree of gland obstruction and destruction you will need to address. By the same token, when your patient sees how terrible their glands look, it is easier to convince them that treatment is necessary, even though most of it is still cash-pay and uncovered by insurance.
It is pretty easy to see “meibomian gland constipation” (hat tip to Preeya Gupta) on imaging. If this is present, your patient requires thermal treatment along with some form of expression. Two instruments will do this as an integrated treatment: LipiFlow (Johnson & Johnson Vision) and iLux (Alcon). You can also use other targeted thermal treatments such as TearCare (Sight Sciences) or MiBo (MiBo Medical Group) and then follow up with manual expression. This is a pretty easy concept both intellectually and operationally: You melt the plug and then open the flow. More than half of our DED patients would benefit.
Our last advanced treatment, but hardly the least, is intense pulsed light (IPL) therapy. First described by Dr. Toyos and subsequently championed by such DED stalwarts as Cynthia Matossian and Laura Periman, IPL treats the inflammation that causes gland obstruction and destruction. Unlike thermal/expression treatments, IPL actually treats the root cause at the anatomic (cautery and closure of telangiectatic vessels), cellular (reduction in release of cytokines and chemokines) and molecular (improved use of ATP) levels. Literally 95% of patients with significant MGD will see both subjective and objective improvement. Nearly every patient with evaporative DED would benefit. Cost to the patient as well as both the capital and ongoing costs (disposables and staff) for the practice are the barriers to moving these therapies into the realm of standard treatments. Still, for any but the most basic DED practices, some version of each of these advanced treatments will need to be available.
Next month we will finish up our series on treating DED with a look at the care of complex cases in “Treating dry eye 401.”
- For more information:
- Darrell E. White, MD, can be reached at SkyVision Centers, 2237 Crocker Road, Suite 100, Westlake, OH 44145; email: dwhite@healio.com.
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