DRY EYE SYNDROME
Signs and Symptoms
Upon gross inspection, the majority of these patients demonstrate a relatively white and quiet eye. However, key slit lamp findings may include a meager tear meniscus at the lower lid, as well as a reduced tear break-up time (TBUT), generally less than ten seconds. Sodium fluorescein staining may be evident as punctate epithelial keratopathy from the interpalpebral region to the lower third of the cornea. In more severe cases, rose bengal or lissamine green staining of the cornea and/or conjunctiva may be seen in the same area. Filaments, which are tags composed of mucus, epithelial cells and tear debris, may also stain with these vital dyes.
Additional clinical tests for dry eye syndrome are numerous. Tear volume assessment is used quite commonly, and may be ascertained by use of Schirmer tear test strips or the Zone-Quick test. Dimin-ished "wetting" of these test media over a set period of time (five minutes for the Schirmer and 15 seconds for the Zone-Quick test) is indicative of tear volume deficiency, a form of dry eye syndrome. Another device, the Keeler Tearscope, utilizes interferometry to evaluate the thickness of the tear film components, particularly the lipid layer. More involved and invasive procedures, including tear film osmolarity, lysozyme analysis, lactoferrin assay, and impression cytology, may be useful in quantifying dry eye for research purposes, but they are hardly practical for routine clinical diagnosis.
Over the last several years, a great deal of research has been conducted in the area of dry eye, revealing startling new information. Of the more intriguing theories is that dry eye may be the result of an inflammatory process within the cornea and/or lacrimal glands.24 This is supported by the fact that pro-inflammatory cytokines and activated T cells have been identified in the lacrimal glands of both Sjögren's and non-Sjögren's patients.5,6 In addition, moderate to severe dry eye states have been seen to respond favorably to treatment with corticosteroids.7 On another front, researchers have shown a significant link between androgens and dry eye.8,9 Apparently, these sex hormones may help regulate homeostasis of the tear secretion process. Women who take hormone replacement therapy with estrogen have an increased incidence of dry eye, possibly due to suppression of endogenous androgens by increased estrogen levels.10,11
Historically, management of dry eye syndrome has been aimed at replenishing the eye's moisture and/or delaying evaporation of the patient's natural tears. The first line of defense typically involves the use of ophthalmic lubricants ("artificial tears"). The purpose of these agents is to alleviate symptoms and, in some cases, to promote healing of the ocular surface epithelium. A great deal of diversity exists within this market, and practitioners should familiarize themselves with the various options (see "Overview of New Dry Eye Products," on page 34A). In general, artificial tears may be used as frequently as necessary, although some are only indicated for qid use. When beginning therapy, they should be dosed frequently (at least every hour), and then tapered based upon patient response and compliance.
Patients who do not respond to palliative therapy may require more substantial treatment in the form of topical and/or oral pharmaceutical agents. The immunomodulatory agent Restasis (0.05% cyclosporine A ophthalmic emulsion, Allergan) has recently been approved by the U.S. FDA "for patients with keratoconjunctivitis sicca ... whose tear production is presumed to be suppressed due to ocular inflammation." Although this topical drug may require bid dosing for up to six months to achieve maximum efficacy, it has been shown to ameliorate symptoms in up to 44% of patients and improve basal tear production (as demonstrated by Schirmer testing) in up to 59% of patients.12
Oral medications and nutritional supplements have been utilized with success for patients with blepharitis and meibomian gland disease, significant causes of evaporative dry eye syndrome. The use of oral tetracycline therapy (e.g., doxycycline 100mg bid x six to 12 weeks) may be beneficial in patients who fail to improve with lubricating drops and lid hygiene. Also, the use of oral omega-3 fatty acid supplements has been suggested as a less invasive way to improve meibomian gland function and tear stability.13
Lacrimal occlusion with punctal or intracanalicular plugs offers a different management strategy for dry eye, essentially preventing drainage of the tear film and maximizing contact duration with the ocular surface. While the theory is sound, a significant percentage of plugs may be spontaneously expelled, and it has been noted that many patients notice a subjective decrease in improvement of symptoms with the plugs over time.14,15 Some individuals have actually cautioned against occlusion therapy in many cases, citing the new inflammatory theories of dry eye; they suggest that the use of punctal plugs actually creates a "cesspool" of cytokines and promotes, rather than alleviates, damage to the ocular surface.16
Patients with keratoconjunctivitis sicca (KCS), a more severe form of dry eye, may not respond to any topical therapy. Often, these patients benefit from oral secretagogues such as Salagen (pilocarpine HCl 5 mg, MGI Pharma) and Evoxac (cevimeline HCl 30 mg, SnowBrand Pharmaceuticals). These muscarinic agonists stimulate non-selective secretion from exocrine glands via autonomic pathways, resulting in enhanced tear production. Typically these agents are used for xerostomia (dry mouth) associated with Sjögren's syndrome or certain forms of cancer. They are utilized by some physicians for advanced KCS; however this is not currently an FDA-approved application of these drugs.
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Neuro-Ophthalmic Disease | Oculosystemic Disease
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