Contact lens-activated inflammation manifests as unsightly conjunctival hyperemia, itching, lacrimation and irritation. The appropriate steps to prevent and manage contact lens-induced inflammation are essential for patient satisfaction and a robust contact lens practice, as when not treated, the outcome is contact lens dropout, disgruntled patients and lost revenue. As a majority of practitioners foresee growth in the contact lens category, as seen in the chart on p.22, there is a chance contact lens-related inflammation could affect larger numbers of patients. Knowledge of the root cause of the inflammatory event will guide the appropriate treatment. Here are several etiologies of contact lens inflammation and methods to mitigate symptoms.
PROTEINS AND BY-PRODUCTS
Buildup of protein deposits or bacterial by-products on a contact lens can induce ocular inflammation via an immune response. This often results from infrequent or improper lens cleaning.
Identify it: You will note these deposits with your naked eye, looking at the lens. They are known as jelly bumps or mulberry spots.
Treatment: This includes more effective cleaning methods, such as hydrogen peroxide-based disinfection systems. Increased lens replacement frequency or a refit to daily disposable contact lenses with a limited wearing schedule should also prove beneficial. This is because extended-wear lenses provide an opportunity for greater accumulation of lens deposits.
Treatment of more severe conditions, such as corneal infiltrates, may include the use of steroid drops and temporary cessation of lens wear.
LID WIPER EPITHELIOPATHY
Lid wiper epitheliopathy is a direct result of surface friction and a further contributor to inflammation. (For more on this clinical condition, see Contact Lens Spectrum’s http://bit.ly/2IQG9TF .)
Identify it: Following instillation of sodium fluorescein and lissamine green dyes, use the slit lamp to examine upper and lower eyelid margins for staining with sodium fluorescein and lissamine green dyes.
Treatment: Contact lens lubricity is a lens attribute that may hold the key to effective treatment. This indicates how “slippery” the lens material is and the degree of friction (measured by the coefficient of friction) it produces. A refit to a lens of greater surface lubricity, along with frequent lubrication with preservative-free artificial tears, may provide relief.
Hypoxic inflammation leads to the formation of sterile marginal corneal infiltrates. Such inflammation induces white blood cells to flood the cornea and stimulate conjunctival hyperemia. Tight fit, excess thickness or low Dk lenses lead to hypoxic conditions.
Identify it: Corneal microcysts, limbal hyperemia, neovascularization, small increases in myopia, discomfort and contact lens intolerance are clinical signs of hypoxic inflammation.
Treatment: Altering the fit and lens material should alleviate recurrence following appropriate medical treatment with topical hyperosmotic drops for edema, lubrication or steroids. High Dk silicone hydrogel lenses are an obvious choice to remediate hypoxia. Additionally, an adjustment in wear schedule is often necessary, as extended wear should be eliminated because closed eye conditions exacerbate hypoxia. As a result, even daily wear use is not always sufficient to eliminate hypoxic events, and wearing time needs to be limited to work hours or recreational use only.
CONTACT LENS SOLUTIONS
Solutions that contain disinfectants and preservatives used for cleaning, soaking and lubricating lenses can create risk to the eye for both toxic and allergic reactions.
Identify it: Marginal blepharitis, superficial punctate keratitis and conjunctival follicles are frequent signs of this induced inflammation.
Treatment: Elimination of offending toxins and allergens is the goal of treatment. Medical treatment of acute reactions with lubricants, antihistamine/mast cell stabilizers, steroids or antibiotics may be indicated. For this patient, consider a change of lens modality to a daily disposable lens down the line. Reason being: Peroxide disinfection systems provide a possible resolution, but not in all cases. Whereas, the use of single-use daily disposable lenses will eliminate solution-based contact lens inflammation and would definitively rule out solution reactions as the source of inflammation.
GIANT PAPILLARY CONJUNCTIVITIS (GPC)
GPC is an inflammatory response to a mechanical or chemical contact lens insult, such as poor contact lens edge and disinfectant residue, respectively. This can occur with any lens modality and may require a refit in the event of a mechanical etiology. For example, excessive lens movement or edge standoff can induce lid inflammation and necessitate a refit.
Identify it: This is a mast cell-mediated reaction that induces papillae in the upper tarsal conjunctiva to coalesce into finger-like projections that perpetuate an endless cycle of mechanical and toxic stress.
Treatment: I begin my treatment with a discontinuation of lens wear. Topical steroids are frequently necessary to break the inflammatory cycle. Adjunctive treatment with antihistamine/mast cell stabilizer drops are indicated and may be used long-term after steroid drops are stopped and lens wear resumed.
DRY EYE DISEASE (DED)
DED appears as a disrupted or destabilized tear film. What happens is that contact lenses may disrupt the tear film by interfering with the adherence of mucin to epithelial microvilli and reducing goblet cell density. A contact lens splits the tear film into pre- and post-lens fractions to further destabilize the tear film. As a result, contact lenses accelerate evaporation of tears, thus creating focal dry spots that lead to ocular surface inflammation. Contact lens wear also is associated with meibomian gland obstruction and dropout — brought on by mechanical stress, alteration of lid microbiome and digital manipulation during insertion and removal — to further decrease tear production and function.
Identify it: To determine DED that results from evaporation, observe TBUT, an increase of which indicates areas of potential desiccation. Additional testing includes gland expression and evaluation of the quality of meibum. Also, realize that the two forms of DED can co-exist.
Treatment: Effective DED treatment to reduce inflammation will often include oral and topical management, and in-office treatments. (For more information on dry eye therapies, see “Defy Dry Eye” in OM, July 2018, https://bit.ly/2JED7Nz .)
Elevated levels of airborne pollutants, such as nitrogen dioxide, and extreme temperatures, result in inflammation that manifests as ocular surface disease. Therefore, those affected complain of irritation, redness, foreign body sensation, tearing and blurring of vision.
Identify it: To find exposed patients, include questions about exposure to climate-induced pollutants and assessment for ocular-related insult in case histories.
Treatment: Reducing exposure is the goal here. Recognition is the first step to avoid inflammatory triggers. Additionally, simple treatment with chilled preservative-free artificial tears may be all that is needed to quell inflammation, but don’t be afraid to bring out the big guns to stabilize the eye when necessary.
Contact lens-induced inflammation is the enemy of successful contact lens wear and a major source of lens intolerance. Appropriate prevention and treatment of inflammation will promote lens comfort and clear vision. Vigilant efforts to detect and control contact lens-related inflammation will prevent patient dropouts and, as a result, increase the number of contact lens patients who will provide a constant referral stream. OM