DRY EYE: It's a Brand New Day
Medical advances have turned an "ophthalmic nuisance" into a condition we can really do something about.
BY CLIFFORD SALINGER, M.D.

It wasn't so long ago that patients complaining of dry eye were a frustrating experience for many ophthalmologists. When patients described their bouts with the "itchy-burnies" we would look forward to, of all things, the next refraction -- hoping that something other than dry eye might explain the problem.

My how things have changed! Today, there's been a resurgence of interest in the diagnosis and treatment of dry eye syndrome (aka ocular surface disease). Many factors have contributed to this:

► Lower reimbursement for surgery has made clinical care comparatively more rewarding. (Today, Medicare pays less than $1,000 for a corneal transplant, and an even smaller amount for a pterygium excision with a conjunctival graft.)

► The incidence of dry eye syndrome following refractive surgery has increased awareness of the problem among both our refractive surgery colleagues and their young urban professional patients.

► The contraction of access to our patient population as a result of insurance-related restrictions requires us to offer a wider scope of services to each individual.

► Most important, better understanding of the ocular surface dynamic -- both in a stable, healthy environment and under compromised conditions -- has led to improved treatments that we can offer our patients. Ever since the mid-1990s, when this condition was redefined as a relative lack of aqueous production combined with an increased evaporative component, we've been better able to manage the problem and better able to educate patients (which can have a dramatic effect on compliance).

Here, I'd like to summarize the highlights of our current array of treatment op-tions, as well as some of the information available to pass on to our patients.

Treatment Alternatives

Thanks to our greater understanding of the problem, we have more treatment options than ever. Some are "tried and true," while others are cutting-edge; but all are helpful, and many are synergistic or additive in their benefits:

Adjust environmental conditions. Environmental exposures and the nature of our patients' daily activities have a significant effect on this condition. This includes the use of some medications such as birth control pills, antihistamines, antidepressants and GI motility medications.

Artificial tears. Advances in our understanding of tear film composition have lead to improved tear substitutes. Use of transiently preserved or preservative-free tear substitutes -- not the generic or BAK preserved preparations -- is very important.

Nutritional therapy. Once dismissed as being akin to voodoo, this has now -- almost -- become part of mainstream medical care. Many doctors were a little surprised when the National Eye Institute's Age-Related Eye Disease Study (AREDS) showed a statistical benefit to high-dose vitamin therapy. We've also been pleasantly surprised by the benefits shown to be associated with the Omega-3 fatty acids found in fish oils, flaxseeds, flaxseed oil and some nutritional supplements. (These benefits are related to the improved rate and consistency of the meibomian gland flow, and better control of the inflammatory cascade.) At the same time, it's becoming apparent that Omega-6 fatty acids, found in ice cream and other dairy products, are not good for ocular surface disease.

When discussing nutritional supplements and dietary changes with your patient, it's important to emphasize the long-term nature of the treatment, and that improvement may take weeks or months to become noticeable.

Hot compresses. Hot compresses help to improve meibomian gland flow and control blepharitis. It's important to instruct patients to use the compresses for 15 minutes (hoping they'll use them for at least 10 to 12 minutes), in order to penetrate and "melt" the inspissated material. This should be followed by a thorough lid hygiene routine, to massage the lids and to remove accumulated debris. (I strongly advise against the use of baby shampoo, a detergent that further destabilizes an already unstable tear film.)

Here again, education is crucial. Patients often find this routine tedious, and if they don't understand how it helps, they'll discontinue the treatments as soon as they feel the least bit better -- and discomfort and irritation will return.

Antibiotic ointment. Used at bedtime, Erythromycin or Bacitracin can improve oil flow by decreasing the population of staph organisms, which in turn allows for a normalization in the esterification of the lipids and a less "soapy" tear film. Continued use will also help to reduce lid margin thickening or hypertrophy (lichenification), which would otherwise further inhibit oil flow.

Medications for inflammation control. These have become more central to our treatment. Research has shown that treatments are palliative at best unless we treat the underlying mechanism responsible for the ocular surface disease.

There are several ways to treat the inflammation:

► A mild or intermediate strength steroid can be prescribed for use two or three times a day, as necessary, to treat the active component of the inflammation.

► Doxycycline is helpful, taken as drops in a specially formulated .025% solution used three to four times a day, or taken by mouth, initially 100 mg p.o. b.i.d. Doxycycline should be tapered -- slowly -- as the condition improves. It may help to control the inflammatory component and, over time, may further improve meibomian gland flow.

► Restasis, the newest addition to our armamentarium, represents a true breakthrough in the treatment of this condition; it may change our entire approach to battling ocular surface disease. Its key ingredient, cyclosporine, mitigates the release of inflammatory mediators (i.e., cytokines) and helps prevent the chemotaxis that encourages lymphocytes to infiltrate the conjunctiva and lacrimal glands.

Inflammation may begin to decrease as soon as 2 to 3 weeks after initiating this treatment. However, increased aqueous (and mucin) production usually takes at least 2 to 3 months to begin. (This takes longer because diseased lymphocytes that alter the normal microscopic anatomy live an average of 110 days; about half die off after 55 days. As the lymphocytic infiltrate recedes, the histology of the lacrimal glands and conjunctiva slowly return to normal.) Meanwhile, the vehicle, an oil emulsion, increases tear film stability with every application.

Punctal occlusion. The benefits of punctal occlusion are well known to many patients and easily understood. Also, the idea of a "quick fix" is very attractive. However, in some cases occlusion may prevent inflammatory mediators from draining away from the ocular surface, making the inflammatory component of dry eyes or allergies worse.

Several modalities now exist for blocking the puncta:

► Plugs that dissolve over time can provide temporary occlusion. (This is a less than ideal test for epiphora, but it can be used if there is any doubt.) We usually use these plugs as a treatment for temporary problems such as dry eye following LASIK, or for corneal abrasions.

► "Permanent" occlusion is available in many forms. Most commonly, silicone plugs with a tapered design and a "mushroom" cap sitting above the surface are well tolerated. Occasionally they may work their way out of position or cause localized irritation, necessitating removal. (This problem is more common in the superior puncta.)

► "Smart" plugs are now available. These are made of an acrylic material that changes shape and size when exposed to body temperature. The plugs begin as long, thin rods (9 mm long by 0.4 mm in diameter). After placement within the canaliculus they shrink to about 2 mm in length and expand to about 1 mm in diameter, pushing against the walls of the proximal canal. In the event of an undesirable amount of epiphora, they can easily be flushed out by irrigating the drainage system.

Educating the Patient

Our expanding knowledge of the ocular surface not only has lead to improved treatments, but also has made us better able to offer a real explanation for the problem -- and specific reasons for our treatment recommendations.

Educating patients is critical. If patients aren't committed to the treatments we prescribe, they won't use them and they won't get better. (And of course, most patients will see the less-than-satisfactory outcome as our fault.) By explaining what's wrong and how the treatment will help to correct it, we make the patient part of the team.

When a patient complains that vision fluctuates shortly after they begin a concentrated visual task, we can now explain that this is a function of tear break-up time or tear film instability, caused by a number of possible factors that they -- and we -- can do something about:

A decreased blink rate. People blink half as often when reading, driving or watching television, and one-third as often when using a computer or concentrating intensely.

Forced air systems (hot or cold). These decrease the ambient humidity, and the air currents they create increase tear film evaporation (as do ceiling fans). We can teach patients to help themselves by emphasizing the importance of environmental exposure and the need to use preservative-free artificial tears and gels frequently.

Decreased aqueous production. This can be caused by many factors, such as the effects of aging and decreased hormonal production (especially testosterone), including peri- or post-menopausal hormone changes and those secondary to pharmacologic agents (i.e., birth control pills). Antihistamines and anti-depressants can also cause decreased aqueous production.

Inflammatory mediators released into the tear film. These destabilize the ocular surface environment and interfere with the neural feedback loop to the lacrimal gland, affecting the signals for output. They also cause chemotaxis, which encourages lymphocytic infiltration of the conjunctiva and lacrimal glands, replacing or obliterating the normal anatomic structures. This further affects production of mucin (conjunctiva) and aqueous (lacrimal glands).

Meibomian gland dysfunction and blepharitis. These problems can further contribute to tear film instability and an inadequate lipid layer. Under-appreciated until recently, they're still not adequately diagnosed or addressed.

We can also help patients understand that fluctuations in vision, such as increasing glare and haloes at night, are related to dryness and the need for more lubrication.

A Change for the Better

Today we can offer these patients much more than we could just a few years ago, and future treatments, such as androgen (testosterone)-containing topical medications, are currently being researched. As with the best of the current medications, these modalities are directed at the underlying mechanisms responsible for the problem. That means they'll help us provide better outcomes for our patients. And, as you know, happy patients refer other patients.

So, we've come full circle. Yesterday's "ophthalmic nuisance" has become today's practice builder.

Dr. Salinger is a cornea and external disease and refractive surgery specialist practicing in Florida in the West Palm Beach and Stuart areas. He received his cornea fellowship training at the Pacific Medical Center in San Francisco, and was associate professor in the Corneal Fellowship program at the University of Rochester. He's also an active participant in the ORBIS International training program, volunteering his services as a teacher in developing countries around the world.