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Cover Focus | May 2015

A New Model for Recognition, Prevention, and Treatment of Dry Eye?

Ophthalmologists can take a lesson from dentists.

We ophthalmologists see a plethora of patients daily who have either clinical signs or symptomatic complaints of ocular surface disease (OSD). It is time all clinicians addressed this disease and made a significant change in the practice of ophthalmology.

If this were the 1890s, and someone told us we had to have the base of our teeth uncomfortably scraped with a metallic instrument, move string up and down in every junction between our teeth, and rinse with fluoride to maintain our teeth, would we believe them? Probably not, because we would not have been educated to understand the pathology of dental decay. Somehow, dentists got the word out, made a career for dental hygienists, and created the primary practice that would feed their larger body of work, all the while saving teeth.

In many instances, dental cleanings are covered by insurance, but often patients pay out of pocket. Moreover, patients begin receiving regular cleanings early in life, and they are conditioned to understand that dental care will help to save their teeth if they follow hygiene instructions.

An adult tooth cannot be regenerated once lost; nor can a meibomian gland. We are just learning that, without providing proper education and understanding, we may be allowing our patients to lose a body part as they age—all because we have not created a model similar to that for dental hygiene. We can visualize the end result of chronic meibomian gland obstruction using new technology (LipiView II; TearScience). With long-term obstruction, the gland dilates, cannot return to its original shape, and eventually atrophies, never to produce oil again. For many patients, our recognition of this cycle is too late.


After getting into treatment of dry eye disease (DED) using artificial tears and cyclosporine ophthalmic emulsion 0.05% (Restasis; Allergan), I added omega-3 supplements (Omega Health; Physicians Recommended Nutriceuticals) to my patients’ regimens, and I realized that they were experiencing a significant improvement in signs and symptoms of DED. The supplements help enhance the composition of the lipids and increase the amount of eicosapentaenoic acid and provide essential natural antiinflammatory nutrients to the entire body. Although I was quite pleased, I knew I still had to do more.

At a Glance

• Surgeons have failed to think about DED as a chronic, progressive disorder of the lids that can be prevented at an early age.
• A paradigm shift in one’s own philosophies and a willingness to take on prophylactic methods of DED management are needed.

More than 3 years ago, Rolando Toyos, MD, introduced me to intense pulsed-light therapy treatments for DED. I was aghast at what I saw inside the glands as I starting expressing them with a cotton swab and my opposing finger after heating them. What was supposed to be a clear substance resembling olive oil was a white, yellow, or brown substance that was more like toothpaste trapped in each gland. How could the ocular surface be properly lubricated when the so-called oil had this thick or globular composition? Additionally, the gland was so blocked that the material could not escape to the surface.

Even with great technologies, we were still letting an important body part die. Douglas Korb, OD, has raised awareness by helping to create the thermal pulsation LipiFlow (TearScience) device. Now, we were able to evacuate the glands in a comfortable manner for patients, but there was still one more component to the puzzle: Why did some people respond well, whereas others had a minimal response if any? What came first, meibomian gland dysfunction (MGD) or inflammation? MGD is present in 86% of DED patients,1 but the concomitant inflammation that coexists once these glands are dysfunctional should not be discounted.

The reason that some patients did not get a significant positive result is that their glands had already either dilated too much or had atrophied. This process begins in early youth, and, unless patients need glasses or contact lenses, they usually do not see an eye care specialist. Additionally, we rarely look at the contents of glands unless someone has chronic chalazia, so abnormal contents build up in the glands with nowhere to go. The lid margin’s surface then keratinizes and externally plugs the meibomian gland orifice, compounding the problem.


We have failed to think about DED as a chronic, progressive disorder of the lids that can be prevented at an early age. Now we face many patients who have chronic irritation and pain and, possibly, loss of vision. The new paradigm should be to educate patients that they need a routine eye physical even if they have to pay for it. Many services coming into our new insurance environment are self-pay, and this should be one of them, as dental hygiene was in the past. Pediatricians and internists should be educated so that they can encourage young people to be examined. When of age, patients should have their lids tested by expression to look for the early dysfunction that we now recognize in 40- and 50-year-olds. Perhaps a simple periodic treatment of lid expression every few years will be enough to stop the blockage of the meibomian ducts.

We can now also perform a multitude of diagnostic tests in the office, including the TearLab Osmolarity System, InflammaDry (Rapid Pathogen Screening), LipiView, Keratograph tear film imaging (Oculus Optikgeräte), fluorescein and lissamine green stains, and the Sjö test (Nicox; not available in Europe).


We may have missed our turn but not our chance to change this chronic disorder for coming generations. It will take a shift in our own philosophies and a willingness to take on prophylactic methods such as early gland evacuation when needed, omega-3 supplements to counteract our Western diet now rich in proinflammatory omega-6, and control of concomitant inflammation with pharmaceutical agents such as cyclosporine. We will need to debride lid margins to release the external keratinized plugs and control the development of Staphylococcus on the margins (as with something like the Avenova lid cleanser [NovaBay]). With awareness of the contributing pathology, we can change the DED paradigm and bring forward a generation that will enjoy ocular comfort and good vision for a lifetime. By being aware of DED, we will be able to utilize all of the great new technologies we have for vision correction. n

1. Lemp MA, Crews LA, Bron AJ, et al. Distribution of aqueous-deficient and evaporative dry eye in a clinic-based patient cohort: a retrospective study. Cornea. 2012;31(5):472-478.

Noel Alpins, FRANZCO, FRCOphth, FACS
• Assistant Clinical Professor of Ophthalmology, University of Maryland
• Founder and Medical Director, Eye & Cosmetic Surgery Center, Mercy Medical Center and the Rowen Laser Vision & Cosmetic Center, Baltimore
srowen10@gmail.com; Twitter @SheriRowen
• Financial disclosure: Consultant (ACE Vision, Alcon, Allergan, Alphaeon, Bausch + Lomb)