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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.
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.
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