No announcement yet.

Hope and new perspective through best-ever diagnostic work-up

  • Filter
  • Time
  • Show
Clear All
new posts

  • Hope and new perspective through best-ever diagnostic work-up

    By way of background, I've had many tough years, but also some very good years, over the course of my 22-year dry eye journey. Reports of many of my successes may still appear here in posts dating back many years.

    I'm back here today to share a breakthrough that comes in the form of a diagnostic work-up so thoughtful and complete that it has dramatically changed my understanding of the processes that turned me into a chronic DES case, and set me on a course toward treatments that may finally help to modify the course of my disease.

    For most of my 22 years with dry eye symptoms that have ranged from mild to disabling, I was operating under the diagnosis of advanced meibomian gland dysfunction. I never pursued some of the newer technologies that provide meibomian gland heating and expression, or gland-cap exfoliation, but was about to seek these out when my symptom picture took a turn for the worse earlier this year. While my symptoms worsened, I also experienced the spontaneous loss of the one punctal plug I'd had in place for 20 straight years, which loss was followed by a series of eyelid infections on the lid where that plug had resided.

    During the first few months of this flare-up, I saw several optometrists, one at a hospital-based dry eye clinic, and they repeated history for me by opining that I have what may be significant meibomian gland failure, and that either because of this, or due to some possible aqueous deficiency, my tear film break-up time was way too short. I was then sent home to try a higher-quality omega oil supplement, do more warm-packing of my eyes, and, perhaps, to ponder whether to move forward with some lid-expression procedure like LipiFlow or TearCare.

    Two pairs of beautiful new moisture chamber glasses later (and these did help to reduce my pain a bit and shield the eyes from too much moving air), my gut told me that I had YET ever to be diagnosed in a methodical way, and that maybe I finally deserved to get the best that modern diagnostics have to offer. But I still believed, as I resolved to seek more diagnostics, that the problem driving most of my symptoms was almost surely a serious failure of my meibomian glands (as this had never been refuted by any doctor I'd seen).

    Enter the optometrist who then produced my quantum leap!

    Last week, I was examined by a local optometrist who has just brought in to his dry eye practice a junior associate who has sought out multiple opportunities around the U.S. to build her knowledge and experience base, and to master all the products and technologies now in circulation for dry eye. As of result of the very memorable exam I received, 1) the pain and periodic disability I've suffered on and off for 22 years were VALIDATED (yay!), and 2) I am now on a course to receive several therapeutics that, for the first time, have the potential to modify the course of my disease for the better.

    In a nutshell:

    New Gross Findings: My doctor instilled flourescein and then, with an optometry resident/student on hand, and narrating what he was doing, stood a foot or so away from me to look at my eyes, under illumination, in order to derive some gross findings. There were two Aha moments: 1) I had NO tear meniscus in either eye, and 2) it was clear that the lower lid on my right eye was lax and not making full contact with the right globe. (My right eye has always been MUCH more symptomatic than my left.)

    Blink videography: Videography of my blinking activity documented that my blink, according to my new doctor, is the MOST inadequate he has EVER seen in a patient. (His words: "You take incomplete blink to whole new levels.") The imaging showed that when I blink, my lids margins NEVER touch, and, in fact, cover only about 10% of the globe on each of top and bottom levels.

    Meibography (and this was my FIRST ever, after receiving diagnoses, all these years, that included "total meibomian gland atrophy/dropout"): Imaging clearly showed only 20% gland atrophy on left eye, and 40% gland atrophy on right eye, constituting findings that the doctor described as "not bad at all," and certainly not sufficient to explain the severity and type of my signs and symptoms.

    No testing for tear osmolarity or inflammatory factors was performed, because this doctor believed (and I agree) that it was already obvious that my tear film is extremely abnormal/deficient in composition and volume, and that my ocular surface had to be quite inflamed as a result of the years of abnormal exposure to which my corneas have have been subjected as a result of the findings already arrived at.

    Based on these findings, and my report of often severe and disabling burning pain, my doctor also concluded that my eyes' prolonged abnormal surface exposure, and concomitant dessication, would have had to cause 1) reduced density of my corneal nerves, 2) corneal desensitization, and 3) overall chronic deterioration of the corneal epithelia. The certainty that my doctor conveyed regarding this was not at all difficult for me to accept. Every fiber of my being quickly understood that there was finally a data-based explanation for everything I've ever suffered.

    An etiology for all this was then posited (and that, too, rang true): When I started wearing rigid, and, later, soft, contact lenses as a pre-teen (and for many years thereafter), to correct for my severe myopia, my blink pattern became inhibited. Over time, lid closer diminished, lacrimal and meibomian secretion diminished, and corneal nerves thinned, leaving the corneas desensitized. The desensitized corneas then became a secondary cause for incomplete and infrequent blinking, which, in turn, and via a feedback loop, 1) somewhat atrophied the function of the ophthalmic (1st branch of the trigeminal) nerve, which ennervates/triggers blinking, and 2) then only accelerated the blink failure (and concomitant lacrimal/meibmomian failures) that was already damaging my corneal surfaces.

    My doctor's associate was willing, moreover, to describe my diagnosis, in etiological terms, as a form of neurotrophic exposure keratopathy (though not the version of this disorder that seems to be genetically determined and very severe).

    Understanding what I do now, I'm willing to venture that I am only one of many millions of dry eye patients whose dysfunction can be explained in similar or even identical terms. . .i.e., terms that include a neurological component that may be central to all the disease's manifestations over time.

    Here's the treatment plan I now have, based on the data and analysis my doctor provided:

    Amniotic membrane grafts for both eyes, with the goal of improving the density of corneal nerves, and, in turn, improving corneal sensitivity and, ideally, blink reflex and resulting lacrimation and meibomian stimulation. Grafts can be repeated periodically as needed.

    Implementation of Dr. Donald Korb's well-known blinking exercise regimen, with assiduous adherence to it henceforth and permanently

    Periodic Blephex treatment to keep meibomian-cap biofilm in check

    Fitting of full-size scleral lenses to inhibit exposure keratopathy for the long haul

    Possible blepharoplasty to tighten the lower OD lid in hopes of eliminating the portion of tear loss that is attributable to the extra surface exposure caused by the lid laxity

    Now I don't yet know how I'll fare with sclerals, but if all goes well, I'll be starting on these fairly soon. . .and it comforts me to know that if, for any reason, these don't work out well for me, I will STILL be able to slow the progress of my disease, and address my symptoms, even just by pursuing grafts, professional meibomian gland maintenance, and, possibly, lower-lid blepharoplasty (which is much less likely itself to trigger ocular surface complications than does upper-lid blepharoplasty)

    For those who've read this far, thank you so much for reading my story to date. . . and thank you, too, if my story has helped to motivate more of us to keep looking for the doctors who really shine and care, and for solutions that can make us far more comfortable and functional than many of us have been for too long.

    <Doggedly Determined>

  • #2
    Thanks for your post!
    I wonder if you, just like me, also suffer from lightly, chronic inflamed eyelids? Is the most inner part part of your eyelid (exterior eyelid, so not inside) more red than the rest of your eyelid; almost as a 'red line' on your eyelids close to your eyelids?

    Side note: keep us updated, I'm curious and interested


    • #3
      I believe I'm in the same boat as you with the decreased corneal sensitivity from years of contact use and asymptomatic dry eye. Have you considered using autologous serum tears every day instead of periodically using amniotic membrane to contribute to nerve growth. This is what Dr. Hamrah prescribes to his Lasik patients with nerve problems and I believe it works a lot better for nerve growth and would be much cheaper as well.

      I don't check these forums very much so if you want any more info just message me on facebook I'm in almost all the dry eye and CN groups as Gabriel Ramsay


      • #4
        Very glad for the interest, Giles and GabeR. I'll continue to post updates here as they develop. In meantime, I don't, Giles, have increased redness on any portion of my eyelids. Instead, I've always had very "injected" (red) palpebral conjunctivae, oddly without ever having any persistent redness on the bulbar conjunctivae. And GabeR, your question about autologous serum reminds me to discuss this with my new optometrist. No ophthalmologist has ever suggested serum for me, even though I've always made a point, to my ophthalmologists, to share that I responded very, very well, in my eyes, to systemic neuropathic pain medications a while ago (which medications were prescribed for me by internal medicine and pain-specialty doctors). . .Now I'm wondering whether my optometrist would have the orientation and prescribing authority to put me on autologous serum. I'm not keen on undertaking the regular lab visits that would come with serum therapy, but I should at least get better educated about this. I also, moreover, have a soft spot for amniotic membrane therapy because my favorite ophthalmologist (Dr. Scheffer Tseng), over the years, was just starting to pioneer development of this therapy (not, then, for dry eye, however) when I moved on after he did all he could do, at the time, to help me. Fifteen years after he popularized amniotic membrane treatment, he published an important paper concluding that this therapy can indeed help regenerate ocular surface nerves, and should be considered a potential mainstay of care for chronic dry eye. There's another concern, for me, about using serum drops: There's only one topical I've ever used that has not worsened my symptoms within minutes to hours after it's instilled, and that one topical is also seriously therapeutic for me (even if not sufficient to normalize my ocular surface). That topical is FreshKote, the only high oncotic pressure drop around, and if I had to use serum drops throughout the day, these could interfere with the hydrodynamic action of the FreshKote on which I depend. I might not have to suspend using FreshKote during membrane grafting, in contrast. That said, though, if serum could stimulate corneal nerve repair to a point at which my tear film became stable without FreshKote, the suspension of FreshKote for serum therapy could be warranted. . .Hmmm . . .Honestly, I am not optimistic that even my wonderful new optometrist will be willing to work out, with me, the medical cost-benefit ratio of trying serum under these circumstances. . . But I will definitely raise the option with him, very much thanks to your excellent question/proposal.
        <Doggedly Determined>