CLINICAL

  the front

Leave Them in Tears

Take a comprehensive approach to managing dry eye disease

JOSH JOHNSTON, O.D., F.A.A.O., ATLANTA

Acouple years ago, an African American female patient in her mid-50s presented with complaints of ocular dryness. Her patient history form revealed she’d seen several optometrists and ophthalmologists for this issue with nine different exams in the past two years, but she could not achieve relief. During the dry eye disease (DED) examination, I briefly left the room. When I returned, the patient was crying and visibly shaken.

“Are you okay?” I asked.

She looked up at me and replied, “Someone finally listened to me.”

At the exam’s end, I diagnosed the patient as having both aqueous deficient and evaporative DED and prescribed the appropriate treatments.

This story illustrates that DED is too often under diagnosed. In fact, the chronic and progressive disease is estimated to affect an estimated 25 million people in the United States. If left undiagnosed, DED will progress, eventually limiting vision and causing symptoms to worsen. In addition, failure to diagnose and effectively treat these patients hinders the financial success of one’s practice.

Here, I discuss the etiology, symptoms, clinical signs, management options, as well as the ICD-9 codes associated with DED.

Etiology

The International Dry Eye Workshop, one of the most comprehensive DED studies to date, reveals that DED falls under two categories: aqueous deficient and evaporative.

Aqueous deficient DED results from the reduced secretion of tears from the lacrimal glands. This form of DED includes Sjögren’s syndrome (primary-aqueous tear deficiency and dry mouth and secondary-primary Sjögren’s coupled with an autoimmune connective disease, such as rheumatoid arthritis) and non-Sjögren’s syndrome.

Evaporative DED results from excessive tear film evaporation from the ocular surface. This form of DED is caused by an intrinsic disease (meibomian gland dysfunction; posterior blepharitis; lid aperture and lid/globe disorders, such as lagophthalmos; and low blink rate) and extrinsic exposure (ocular surface disorders, such as a vitamin A deficiency; allergic conjunctivitis; contact lens wear; tear film instability; goblet cell loss and exposed ocular surface disease). Patients can have both aqueous deficient and evaporative DED and oftentimes there is overlap with most patients exhibiting both forms.

DEWS lists the following common risk factors for DED: increasing age (weakened immune system); anticholinergic drugs (antihistamines, tricyclic antidepressants, etc.); poor diet (low water intake, excess caffeine and/or alcohol intake, low amounts of fatty acid intake, etc.); heating/cooling systems (they decrease humidity); changes in hormones (chronic androgen deficiency, menopause and hormone replacement therapy); cancer (systemic chemotherapy, ocular graft vs. host disease and radiation therapy); previous ocular surgeries, such as LASIK (there can be damage to the corneal nerves, disrupting the neural feedback loop); contact lens wear; and digital display use (fixation can reduce blink rate).

DEWS II will begin soon and is estimated to take 18 months to complete. Specifically, the study will update the definition, classification and diagnosis of DED, critically assess the etiology, mechanism, distribution and global impact of this disorder and address its management and therapy.

Symptoms

► Dryness

► Burning

► Stinging

► Foreign-body sensation

► Grittiness

► Blurred or fluctuating vision

► Fatigue

► Itching

Clinical signs

► Redness

► Hyperemia

► Conjunctival staining

► Decreased TBUT

► Increased osmolarity

► Increased inflammation

► Decreased aqueous production

► Meibomian gland obstruction

► Meibomian gland atrophy

► Decreased meibum production and secretion

Management options

To determine the best management option(s), you must pin down the contributing factors. This requires diagnostic testing in the form of a case history; fluorescein staining (under blue light to view corneal staining and decreased TBUT time); lissamine green or rose bengal staining (viewed under white light to see conjunctival signs); osmolarity testing; meibography; tear assessment of lactoferrin and IgE; lipid layer analysis with an interferometer; quantity and quality of meibomian gland secretion via manual meibomian gland expression; MMP-9 and inflammation detection; OSDI, SPEED questionnaires, Schirmer and phenol red thread test; topography; and slit lamp photo assessment.

DED management is comprised of the following:

► Environmental changes. If the case history reveals computer work and a workstation located near heating/air conditioning ducts, recommend these patients keep their computer monitors below eye level, which will reduce the exposure of the corneal surface and decrease the rate of evaporation of the tear film; take regular breaks from near tasks; increase water intake; decrease alcohol and caffeine consumption; and use nighttime moisture goggles and a humidifier by the bed or near their environment. Also, recommend the patient practice consciously blinking to promote tear production and release of meibum from the meibomian glands.

► Nutritional supplements. Studies have shown EPA, DHA, GLA, omega-3 and omega-6 all work to decrease ocular surface inflammation, increase tear production and improve meibomian gland secretions.

► Altering dryness-causing medications. If you think systemic drug use may be contributing to DED symptoms, consider speaking with patients’ primary-care physicians about the possibility of altering or decreasing the use of these medications.

► Artificial tears. These offer short-term relief. For aqueous deficient DED, many advanced technology tears are available that provide relief. If evaporative DED is the main cause, use a lipid-based artificial tear to supplement the missing lipid layer. Also, nighttime ointments work well in patients who have lagophthalmos and incomplete nocturnal lid closure. When relief is needed more frequently for both aqueous deficient and evaporative DED patients, recommend a more viscous tear or a non-preserved artificial tear to prevent corneal toxicity.

► Immunosuppressive topical drops or ester-based steroids. These work well in treating the inflammatory component of both types of DED. I prescribe an immunosuppressive drop if patients are using artificial tears more than twice a day, have corneal or conjunctival staining, and I adhere to the recommendations of the International Task Force Guidelines when determining treatment plans using these medications.

► Autologous serum drops. These are ideal for more severe cases of both aqueous deficient and evaporative DED patients because they contain the same naturally occurring substances of normal tears, which have been shown to work better than synthetic artificial tears.

► Oral cholinergic agonists. These have been known to relieve symptoms of dryness, while improving aqueous tear production.

► Amniotic membranes. These help decrease inflammation and promote healing in patients who have severe aqueous deficient and evaporative DED.

► Punctal occlusion. Consider this treatment after inflammatory cells in the tear film and on the ocular surface have been treated with immunosuppressive drops for three months. Tears without inflammatory cells will start being produced, as T-cells, and other inflammatory cells have a life cycle of around 100 days.

► Lid hygiene. In patients who have evaporative DED, prescribe heating the lids with eye masks, followed by lid scrubs and lid massage to clear clogged meibomian glands.

► Meibomian gland expression/probing. Both actions clear abnormal meibum from meibomian gland orifices in patients who have evaporative DED, though the latter is more invasive, as a probe is used post-topical anesthetic.

► In-office procedures. These evacuate the meibomian glands with automated heat and pressure.

► Oral tetracyclines. These are ideal for posterior blepharitis (evaporative DED), as they decrease bacteria and improve tear film quality.

► Antibiotic and/or steroid. Used either as topical drops or ointments, they improve the meibum’s quality and help increase secretion.

That patient

The aforementioned patient was able to achieve symptom relief and continues to be my patient today. Allergic conjunctivitis can greatly affect our patients’ quality of life, especially contact lens wearers. Let’s actively identify and educate these patients that we have the skill and prescription rights to provide relief. OM

Dr. Johnston practices at Georgia Eye Partners. He focuses on ocular surface disease and has extensive experience in comanaging cataract and refractive surgery patients. E-mail him at drj@gaeyepartners.com, or visit tinyurl.com/OMcomment to comment.