Keratitis: A Contact Lens Dilemma
BY HARVEY M.
ROSENWASSER, OD, FAAO
Punctate keratitis (PPK) is an asymptomatic, treatment-resistant punctate staining of any area of the cornea, although most common inferiorly, of unknown etiology. It typically presents OU but may be monocular. It may go into remission or exacerbate for weeks or years.
PPK is most commonly seen in patients with some limbal and bulbar injection and minor contact lens discomfort and is most prevalent in soft lens wearers. It persists when lens wear ceases, and the patient becomes asymptomatic; it worsens to the point of intolerance with lens wear.
Some reasons for corneal staining include ocular allergy, dry eye, meibomian gland dysfunction, blepharitis including staph lid disease and exotoxins, bacterial and viral conjunctivitis, lens solution toxicity and hypersensitivity, and even medications used for treatment of these.
I have seen cases that will not respond to one just treatment. Although cessation of eye make-up use and contact lens wear and use of non-preserved lubricants, NSAIDs, mast cell stablizers or antibiotics may help, they typically do not. In symptomatic cases, steroids will suppress the discomfort but the symptoms will return when use is discontinued.
When the patient is symptom-free but PPK has been observed, rapport can be challenging because the patient assumes the problem lies with the lens. Patients need to understand the staining is present whether lenses are worn or not. Some patients probably discontinue lens wear due to a vague intolerance. In some cases, the clinician may be misled into thinking the treatment was successful only to find that treatment no longer works when the PPK returns.
PPK Case Example
Recently, a 43-year-old, long-term contact lens wearer presented with PPK after attempting to return to lens wear after kidney and pancreatic transplant surgery. Although she had previously worn soft bifocal lenses successfully, she now reported discomfort, redness and lens intolerance. She had no blepharitis or meibomian gland disfunction and no indication of dry eye by tear break-up time or Shirmer test. The PPK persisted despite use of non-preserved lubricants, lid soaks and scrubs, anti-allergy drops, bacitracin and anti-virals. As a result of her surgery, she was taking 40 pills per day. One wonders if her immune system suppression from the anti-rejection drugs may have contributed to the PPK.
I find a 40 percent prevalence of preauricular adenopathy in PPK patients. These patients typically have no cough or coryza. Some patients admit to a recent "cold," but they do not report it at the time of the examination. These patients are typically not symptomatic when their contact lenses are worn. One case reported by Darougar isolated adenovirus in a corneal scraping in a monocular keratoconjunctivitis case that lasted 16 months. The virus was isolated one year after the onset of the symptoms. It is interesting to speculate that PPK may be caused by past inflammations, infections, or autoimmune diseases that have run its course is no longer clinically evident except for the PPK. Most clinicians would put staphylococcal exotoxin hypersensitivity high on the list, along with adenovirus with the presence of HLA-DR 3 or some other histocompatibility antigens which may account for
For now, PPK remains a perplexing and annoying for both practitioners and patients.
Dr. Rosenwasser is Vice-President of the Societie d'Optometrie d'Europe and serves on the visiting staff of The Eye Institute of the Pennsylvania College of Optometry. He is a moderator of
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Contact Lens Spectrum, Issue: December 2001