Dry eye syndrome is a chronic, complex, and potentially debilitating condition that affects millions of Americans each year. To begin to make sense of dry eye (DE), we must first understand the definition. The Dry Eye Workshop (DEWS) classified DE as “a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability, with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.”
One article is hardly enough to cover all aspects of DE, so Part 1 of this 3-part series will briefly describe background information, pathophysiology, signs, and symptoms.
Background: Let’s start by breaking down the tear film, the common denominator among DE and other ocular surface abnormalities. The tear film functions primarily to provide a clear refractive surface, nourish the cornea, and remove debris. The three layers that compose the tear film are:
- The outer lipid layer reduces tear evaporation. It is secreted by the meibomian glands, glands of Moll, and glands of Zeiss.
- The middle aqueous layer nourishes the cornea, removes debris, and contains protein, lysozymes, and lactoferrin (anti-bacterial). It is secreted by the lacrimal gland, glands of Krause, and glands of Wolfring.
- The inner mucus layer spreads the tears onto the ocular surface. It is secreted by goblet cells and corneal epithelial cells.
Now, let’s divide DE into different subtypes:
- 1) Evaporative: Tears evaporate too quickly
- 2) Aqueous-deficient: Insufficient tears produced; includes Sjogren’s Syndrome (an autoimmune disease characterized by dry eyes, dry mouth and/or arthritis) and non-Sjogren’s (typically involutional changes)
- 3) Combined evaporative and aqueous-deficient form
Although the categorization of DE shown above appears to be falling out of favor, it still serves as a useful general guideline.
As stated in the DEWS definition, DE is a multifactorial condition, signifying that multiple components play a role in the development and progression of DE. We can distinguish between intrinsic and extrinsic factors:
- Intrinsic Factors: Meibomian gland dysfunction, low blink rate, lid abnormalities, etc.
- Extrinsic Factors: Vitamin A deficiency, contact lens wear, allergy, drug preservatives, etc.
Also remember that DE is a leading cause of contact lens dropout!
Pathogenesis: In DE there is release of cytokines, MMPs, and other inflammatory molecules. For a (very) simple schematic, look no further!
- Unstable/poor quality tear film –> Increased tear evaporation –> Increased tear osmolarity –> Inflammation
Symptoms: As will be discussed in Part 2 of this 3-part series, diagnosing dry eye syndrome and assessing DE status can be difficult. Some factors that can contribute to the diagnostic challenges are the severity of DE symptoms (which can range from mild to severe) and the transient nature of symptoms. Sometimes patients complain that their eyes are as dry as the desert but their anterior segment appears clean as a whistle. While other times slit lamp examination reveals 90% meibomian gland inspissation, superficial punctate staining and lid telangiectasia, only for a patient to tell you that they’ve never experienced any eye discomfort! In other words, patient symptoms and clinical exam findings do not always correlate. A non-exhaustive list of commonly reported symptoms is shown below:
- Blurry vision
Signs: There are multiple ways DE can present in your chair. A few are listed here:
- Staining of the cornea, conjunctiva, and/or eyelids after instillation of dye
- Conjunctival hyperemia
- Tear film abnormalities (foam, filaments, etc.)
- Meibomian gland inspissation
- Telangiectasia of the lid margin
Key Points: It is very important to understand that in regards to ocular surface disease, DE is just one piece of the puzzle, along with meibomian gland deficiency and other abnormalities. Additionally, the underlying mechanisms of dry eye are still under investigation. Hopefully the DEWS2 report (set to be released May 2017) will expand our ever-growing knowledge about this chronic condition.
Stay tuned for Part 2 of this 3-part series in which clinical tests, challenges, and new research will be discussed. If you have any questions, please feel free to leave a comment below!
About Chris Lopez
A third year OD/MS student at the University of Houston College of Optometry, Chris holds multiple positions with OptometryStudents.com: Director of Academy Relations, Executive Editor, and Executive Journalist. He is President of Beta Sigma Kappa, Past-National Liaison of the American Optometric Student Association, and is completing his thesis on new diagnostic tests for ocular surface disease. In his personal time, Chris enjoys playing guitar and spending time with his wife Samantha.