Treatment Plan

“The Past Is Prologue…”— Never Truer than for Dry Eye

Treatment Plan

“The Past Is Prologue…”— Never Truer than for Dry Eye


The definition of “dry eye” has been applied to dry eye disease (DED) (American Optometric Association [AOA], 2016), meibomian gland dysfunction (Nichols et al, 2011), and various forms of blepharitis (Lindsley et al, 2012). While the context is different from William Shakespeare’s The Tempest, etiologies and characterizations have become more refined over the past three generations, and new and better treatment strategies continue to be introduced.

A Look Back

Tear Osmolarity Looking back to some of the seminal work on the tear film, Gilbard et al (1978) identified increased osmolarity among his keratoconjunctivitis sicca patients. Today, we can test tear osmolarity easily in a much simpler way compared to the past spectrophotometric analyses that required samples collected during overnight hospital stays.

Knowing tear osmolarity is suggested to allow a stratified treatment approach based on clinical guidelines developed by the Tear Film & Ocular Surface Society Dry Eye WorkShop (DEWS) group (Foulks et al, 2009; DEWS, 2007; Lemp and Foulks, 2008); this group set out to classify the disorder based on clinical findings and the presumption that inflammation is a component deserving attention. Clearly, while this is a big step in the right direction, osmolarity is not the whole picture.

Blepharitis Lindsley et al (2012) concluded that no definitive evidence for any treatment to cure chronic blepharitis exists. Evolving classifications that began nearly 70 years ago now offer some options for treatment beyond the palliative pillars of lid hygiene and tear supplementation (Thygeson, 1946). Researchers have assimilated clinical trial data and laboratory investigations to provide good evidence for pulsed topical steroid treatments to minimize the inflammatory component attributed to patients diagnosed with DED (AOA, 2016; Nichols et al, 2011; Lindsley et al, 2012, DEWS, 2007; and others. Full list available at

A Look Forward

Future DED treatment may include novel compounds, such as lifitegrast (Shire), which has been shown to relieve symptoms in patients who have moderate-to-severe DED (Holland, 2016) by targeting key inflammatory cytokines, thus preventing the downstream cascade associated with DED (Shire, 2016). The U.S. Food and Drug Administration is scheduled to rule on lifitegrast by the end of this month.

At this year’s Association for Research in Vision and Ophthalmology (ARVO) meeting, pterostilbene, an anti-inflammatory compound derived from blueberries, was reported to reduce oxidative stress on cultured corneal epithelial cells (Li et al, 2016). The mechanism appears to be inhibition of inflammatory molecules such as cyclooxygenase 2 (COX-2), a well-characterized enzyme involved in the inflammatory cascade, which has been shown to be blocked by corticosteroids. Unfortunately, chronic topical steroid application has too many local adverse side effects for continual use. While still well away from human clinical trials, this compound may offer another avenue for DED treatment.

Another item is the combination of carboxymethylcellulose in combination with hyaluronic acid for patients who have both aqueous deficient and evaporative dry eye. In both patient groups, clinical signs and patient symptoms improved (Simmons et al, 2016). We have more options at our disposal now than ever before. CLS

For references, please visit and click on document #248.

Dr. Semes is a professor of optometry at the UAB School of Optometry. He is a consultant or advisor to Alcon and Allergan, and he is a stock shareholder in HPO.