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Archivos de la Sociedad Española de Oftalmología

versión impresa ISSN 0365-6691

Arch Soc Esp Oftalmol vol.79 no.12  dic. 2004






It is perplexing that there is not better correlation between subjective symptoms and objective findings in patients with dry eye (1,2). This may lead one to conclude that either there is no correlation or our methods for eliciting historical information, clinical examination, and clinical testing are not sufficiently sensitive and specific for diagnosing the dry eye. However, another conclusion is possible. It may be that part of the difficulty is in our definition of dry eye. What is a dry eye? Is it just subjective symptoms or are objective findings necessary to prove the diagnosis. If the definition is based solely on symptoms then resolving patient symptoms is our only goal in treatment. If, however, we require the presence of objective findings in addition to symptoms, then our therapy is aimed at resolving both objective findings and symptoms. The dry eye, as defined by the National Eye Institute Workshop is «a disorder of the tear film due to tear deficiency or excessive evaporation which causes damage to the interpalpebral ocular surface and is associated with symptoms of ocular discomfort» (2). Dry eye was also classified into two major categories, aqueous deficient and evaporative. While this definition and classification of dry eye was useful at the time, recent information shows that ocular surface inflammation plays a critical role in the etiology of dry eye symptoms and findings. In dry eye subjects treated with the immunomodulatory agent cyclosporin A, there is a reduction in the number of activated conjunctival lymphocytes (3). Furthermore, treatment with topical steroids results in improvement patient symptoms and objective findings (4).

Clinically, it is more useful to classify dry eyes into inflammatory and non-inflammatory causes. This allows one to determine if a patient needs topical anti-inflammatory treatments. How, then, does one diagnosis the presence of ocular surface inflammation based on clinical examination and with the clinical tests that are routinely available to the practicing clinician?

Asking the patient questions such as are your eyes dry, do they feel like sand or gravel, do they burn are useful, although they do not assess the affect of dry eye on the daily living. A recent study using a patient questionnaire and normal office-based clinical examination and testing showed correlation of clinical findings with patient symptoms later in the day but not with morning symptoms (5). In my experience, if one is to rely on a single question, asking, «do your eyes feel like there is sand or gravel in them, especially in the later afternoon?» is the best one to ask. Be wary of patient descriptions of discomfort that do not include the words «sandy, scratchy, burning, irritation something in my eye» as lack of these symptoms suggests something other than ocular surface induced discomfort. Another important point is that patients with chronic eye inflammation due to dry eye seem to complain of less discomfort than one might expect based on clinical examination. With appropriate anti-inflammatory treatment symptoms often worsen before they improve. This may be related to an inflammation-induced hypesthesia of the ocular surface.

In a busy clinical practice one must rely on the clinical exam and readily available clinical tests to determine the presence of ocular surface inflammation in the dry eye patient. Often, blepharitis, in particular meibomian gland dysfunction, is present in patients with an aqueous deficient dry eye and may be a cause of ocular surface inflammation. Findings associated with meibomian gland dysfunction include the presence of oil droplets on the lid margins, foam along the eye lid margin, plugging of the meibomian gland orifices, difficulty in expressing meibum, toothpaste like meibomian gland secretions, erythema and increase vascularity of eyelid margin, and eyelashes growing out of the meibomian gland orifice.

Clues to the presence of conjunctival inflammation in the dry eye patient include redness and injection of both the bulbar and palpebral surfaces and a papillary reaction of the bulbar conjunctiva. The papillary reaction tends to be more prominent on the bulbar conjunctival surface.

More significant inflammation will result in damage to the cornea and conjunctival epithelial cellular membranes. This presents as a punctate epitheliopathy with punctate erosions of the cornea and conjunctiva. Fluorescein staining occurs when there is epithelial cellular membrane and cell-to-cell disruption. Punctate corneal and conjunctival staining in the dry eye patient suggests the presence of inflammation. In the dry eye patient, inflammation leads to increased debris in the tear film and precipitation of mucin. The presence of punctate erosions and precipitated mucin can lead to mucin deposition on the cornea (mucin plaques) and filament formation. The presence of filaments on the exposed interpalpebral cornea results from decreased aqueous tear secretion, inflammation, and incomplete eyelid blinking.

Clinical tests that are readily available are useful in determining the functional status of the lacrimal gland, the stability of the tear film, and status of the protective mucin-tear gel. These include the Schirmer 1 and 2 tests, fluorescein breakup time (FBUT), and ocular surface staining with rose Bengal or lissamine green. The Schirmer 1 and 2 (Schirmer 1 with nasal stimulation) tests are useful in determining the functional status of the lacrimal gland. An abnormal Schirmer 1 test (< 5mm wetting/5") and an abnormal Schirmer 2 test suggest lacrimal gland disease (most commonly due to an autoimmune disease such as Sjogren's syndrome). An abnormal Schirmer 1 test and a normal Schirmer 2 test suggest that the lacrimal gland is still functional (normal Schirmer 2 test) but there is a relative hypesthesia of the ocular surface and lack of afferent stimulation of the lacrimal gland (abnormal Schirmer 1 test). An abnormal FBUT (< 10 seconds) occurs in moderate to severe aqueous tear deficiency, ocular surface inflammation, and meibomian gland dysfunction. Rose Bengal stains epithelial cells when the protective mucin layer is absent or abnormal. Although lissamine is a vital dye, its staining characteristics are similar to rose Bengal. None of these clinical tests is specific in identifying ocular surface inflammation, but are helpful in determining if an aqueous deficiency is present. Until more practical and clinically useable tests are readily available, it is the clinical examination that is most important and most useful in determining the presence of ocular surface inflammation.

So is the diagnosis of dry eye a diagnostic or definition dilemma? Actually it's both.

1MD. Professor Department of Ophthalmology. University of Minnesota. Minneapolis, MN. Associate Medical Director. HealthPartners Medical
Group. Minneapolis, MN.


1. Schein OD, Tielsch JM, Munoz B, Bandeen-Roche K, West S. Relation between signs and symptoms of dry eye in the elderly. Ophthalmology 1997; 104: 1395-1401.

2.Lemp M. Report of the National Eye Institute/Industry workshop on Clinical Trials in Dry Eyes. CLAO J 1995; 21: 221-232.

3. Kunert KS, Tisdale AS, Stern ME, Smith JA, Gipson IK. Analysis of topical cyclosporine treatment of patients with dry eye syndrome: effect on conjunctival lymphocytes. Arch Ophthalmol 2000; 118: 1489-1496.

4. Marsh P, Pflugfelder SC. Topical nonpreserved methylprednisolone therapy for keratoconjunctivitis sicca in Sjogren syndrome. Ophthalmology 1999; 106: 811-816.

5. Begley CG, Chalmers RL, Abetz L, Venkataraman K, Mertzanis P, Caffery BA et al. The relationship between habitual patient-reported symptoms and clinical signs among patients with dry eye of varying severity. Invest Ophthalmol Vis Sci 2003; 44: 4753-4761.

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