Treating dry eye 401: A master class in treating complex cases
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If you have made it through the Level 101 introduction course on dry eye disease diagnosis, Level 201 on the basics of treating DED and Level 301 on using advanced therapies for patients who require them, you are ready for a master class.
This month we bring to a close our four-part series of all things DED by reviewing how one might address some of the most complex and challenging cases. Mind you, even if you have a very advanced DED center, it is perfectly reasonable to choose not to treat the most difficult variants of DED. Doing so can be awfully tough sledding, indeed.
But if you are game, here we go.
This stage of DED care largely comes down to two categories: severe symptoms without signs and severe signs with little to no symptoms. Let us begin with the latter because in many instances this type of “dry eye” often requires the kind of help that we, as eye doctors, really do not offer. Sometimes referred to as neurogenic DED, these patients arrive in the office depressed and defeated. You may be the third or fourth or eleventh doctor they have seen. This makes sense; without any significant signs or abnormal test results, it can be confusing when a patient complains of some or all of the classic dry eye symptoms. Even more troubling, many in this group of patients will have symptoms that generate a SPEED score higher than 25 or an OSDI that approaches 100.
Digging a bit deeper into the patient’s history is always helpful; you may find that they actually did have classic DED signs and lab results once upon a time. With or without this information, if they have any of the classic rheumatologic diseases we associate with DED (lupus, Sjögren’s, rheumatoid arthritis, etc), you will feel like you are on the right track. A history of migraines of any type is a tip-off that they may be susceptible to central pain syndromes. This is especially true if they suffer prolonged migraine episodes.
First you must determine if a patient still has peripheral pain stimuli or if they are suffering from a pure central pain syndrome caused by inappropriate impulse firing in the pain centers of the brainstem. There is really only one unique diagnostic test to remember in these circumstances, the topical anesthetic challenge. I ask the patient to concentrate on their discomfort and to give it a pain value of 50. Approximately 5 minutes after instilling a topical anesthetic, I then ask them to revalue their pain. More than 50 is worse, less is better. If they do not appreciate a decrease in their discomfort, you can assume that their pain is neurogenic.
No additional external therapy will improve their symptoms. While you should continue to treat the ocular surface in order to make sure there is no new peripheral stimulus, this patient should be referred to a collaborative team that includes neurology, pain management and perhaps psychiatric specialists. Treating central pain syndromes is beyond the reasonable scope of care for pretty much all of us.
Patients with the opposite profile, those with signs that vastly outstrip symptoms or those with severe signs and symptoms that resist resolution with even advanced treatments, can also present a formidable challenge. The trick with these patients is to determine if they have reduced or absent peripheral nerve sensation. When you see signs of severe dryness and/or inflammation that is not responding to aggressive treatment, you should test them by touching the cornea with anything that would typically elicit sensation. You do not need to be fancy; a short piece of dental floss or a wisp of cotton will do. No sensation equals neurotrophic disease.
By and large, with or without neurotrophic disease, what you are dealing with in these cases is severe inflammation that has not responded to treatment. Immunomodulators, with or without steroids, have failed you and your patient. Appropriate implementation of office procedures such as LipiFlow (Johnson & Johnson Vision) or TearCare (Sight Sciences) and intense pulsed light have not solved the problem. You look at their corneas, and you see potato chips. There is so much staining it looks like those photos of the Milky Way from the Hubble space telescope.
The easy button is autologous serum tears. Although they are not covered by insurance, they are widely available and not terribly expensive. We use Vital Tears from a subsidiary of the eye bank in St. Louis (hat tip to Gregg Berdy, MD). One can also consider Regener-Eyes, an engineered “biologic” derived from placental material. This comes in two strengths and contains a plethora of anti-inflammatory cytokines and chemokines, as well as growth factors to encourage cell repair. Regener-Eyes does not require a blood draw and is somewhat less expensive than serum tears. There is also interesting work being done using drops made from platelet-rich plasma, the stuff that gets injected into the joints of your favorite NBA shooting guard.
When it really hits the fan, you will have to call out the big guns. If there is any corneal sensation remaining, my first instinct is to place an amniotic membrane “contact lens” on the affected cornea. There are fans of both cryopreserved and freeze-dried options. We have had success with the various options in the ProKera line (Bio-Tissue). These are on label for severe keratitis of all kinds. Beware, they almost always require a preauthorization. In cases of true neurotrophic corneas, the introduction of Oxervate (cenegermin-bkbj ophthalmic solution 0.002%, Dompé) has been a true game changer. A 6-week course of Oxervate often turns these cases around. If there is still residual inflammation, you can repeat the treatment. This, too, almost always requires a preauthorization. The line between true and pseudo-neurotrophic corneas is probably not significant. You could easily use each of these treatments in either circumstance and could follow up a course of one with the other in particularly rough cases.
There you have it, a curriculum for developing a DED program. Beginning with diagnostics and moving through basic, advanced and complex treatment options, The Dry Eye course presented will give you what it takes to begin treating DED. Whether you are an MD/DO or an OD, there are many who have traveled this road before you who will gladly be your guide. The unmet need for DED doctors remains huge. However difficult it can be to treat patients with DED, the successes are among the most satisfying in all of medicine.
- 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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