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February 16, 2021
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Treating dry eye 101: Making the diagnosis

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Here we are on the cusp of a new decade. There are all kinds of new things in literally every pipeline in eye care.

As it has been for at least 10 years, dry eye disease remains fertile ground for growing new products, especially those that will treat both signs and symptoms of DED. After the introduction and rapid uptake of new ways to diagnose DED over the last decade, there is not much going on in that domain. Think of diagnostics as a previously productive bit of farmland lying fallow for a bit. Still, with so much happening on the therapeutic side, this is a good time to review how we should be approaching DED today.

Darrell E. White, MD
Darrell E. White

Let us start with making the diagnosis. When someone comes to your office, you need to determine if they might have DED and start the diagnostic process. Next up, what kind of DED does your patient have? Your initial treatment will be driven in large part by whether you feel the predominant DED type is aqueous-deficient or evaporative. Are there signs of inflammation, and if so, from where does it appear they are emanating? Finally, is there other data that you can acquire and evaluate that will allow you to further define both the type of DED and its underlying pathophysiology?

Anyone in the office can initiate an evaluation for DED simply by being alert to typical symptoms shared at some stage of an appointment. A practice interested in caring for these patients should empower everyone, from the person answering the phone through the technician doing a pretest, to push “go” on a DED protocol. Our patients will tell us if we listen carefully enough. Burning, tearing, and blurred or fluctuating vision are all symptom tip-offs. Indeed, the most common symptom that a DED patient shares at some point in their journey is — wait for it — “My eyes are dry.” Asking a patient if they take eye drops is also helpful; the likelihood that they have DED if they are taking any over-the-counter drop whatsoever is off the charts high.

Beginning with the introduction of the Ocular Surface Disease Index (OSDI) developed by Allergan, the use of patient screening questionnaires is a way to “objectify” what patients are experiencing. In so doing, we create an integer that can be used to compare symptom severity from visit to visit. This is the same with other patient questionnaires such as Standardized Patient Evaluation of Eye Dryness (SPEED) and Symptom Assessment Questionnaire in Dry Eye (SANDE), as well as simpler visual or symptom analog scales that ask a patient to assign a numeric score to the severity of their overall experience. If you drill down into the nitty-gritty of these surveys, especially OSDI and SPEED, you can uncover details that give you a sense of the specific diagnosis you will make. For example, morning discomfort is strongly associated with meibomian gland dysfunction-driven evaporative DED.

Once it is clear that it is likely that a patient has some kind of DED, it is possible to order point-of-care testing if it is available in your clinic. Mind you, there are some prominent DED doctors, doctors who are thoughtful, who disagree with me on this, at least in part. However, I continue to feel that these tests are helpful if they are available in your clinic. Tear osmolarity (TO), at the moment only available in the U.S. from TearLab, is a valuable metric. Elevated TO (greater than 308) in either eye is diagnostic for DED, as is asymmetry greater than 8 mOsm/L between the eyes. Note that this applies even with TO less than 300. Likewise, it is helpful to ascertain the presence of increased MMP-9 activity on the ocular surface. Again, only one test (InflammaDry, Quidel) is available at this time.

More advanced clinics will go on to image both the meibomian glands and the tear film itself. Few things in dry eye are more impactful than showing your patient how terrible their glands look. Mine are ready to jump out of the exam chair and ask when they can have intense pulsed light or LipiFlow (Johnson & Johnson Vision) when I turn the images (that they have already seen) toward them to explain. While we do not have this capability, I imagine that it is similar when you show a video of rapid tear film breakup. Most patients understand the concept of tear breakup time, but I will bet that they accept your findings more readily if they see it themselves.

All of this can occur before you even step into the exam room and take your seat in front of the computer to begin your APOS note. Once you move to the slit lamp, it is time to fill in the rest of the blanks as you start to formulate your action plan. There is nothing fancy about this; your slit lamp exam is the blocking and tackling of anterior segment eye care. Lids, conjunctiva, cornea. What did the Staar Chamber say? Push, pull, lift, to which I would add “look down to see if there is cylindrical dandruff on the lashes. Are there telangiectatic vessels on the lid margin? Push on the lid margin and take a look at what comes out.

I like to look at the ocular surface before I put any type of dye in if I can. When the patient blinks and the conjunctiva moves, that eye is dry. Seriously, I can almost hear the conjunctiva squeak. If you see punctate keratopathy on the cornea before using any dye, that eye is really dry. Now put in fluorescein. Check the staining pattern. Count out tear breakup time. As I have said many times over the years, all you have to do is use fluorescein, and you can make the diagnosis of DED and determine if treatable inflammation is present. Having said that, all of my colleagues who have enjoyed dancing on my head at meetings because I pooh-pooh the need for lissamine green are mostly right; when you stain with lissamine green, mild DED is often unmasked as the severe DED it really is. In addition, a quick smartphone picture of lissamine green staining is impactful when shown to a patient.

I stand by my prior statements on rose bengal: The only reason to use it is to show off that you know it is ben-GAHL and not BENG-al.

And there you have it. You have diagnosed DED, you have the data to determine the type of DED, and you have evidence for the presence or absence of inflammation that can be treated. Next month in “treating dry eye 201,” we will tackle the challenge of determining an initial treatment plan based on the most basic information gathered in our exam.