A common finding in patients who suffer from dry eye disease (DED) is punctate epithelial staining with fluorescein. These individuals may, or may not, be symptomatic.¹

Even though the use of fluorescein dates to the 1880s, the exact mechanism(s) of factors contributing to the staining of cells remains a matter of assumptions rather than hard, clinical facts.² There is even some controversy as to whether cells must first be damaged in order to absorb this “vital” dye. Factors such as concentration, thickness of the fluid layer, pH, and even the wavelength of the light used to excite the dye may alter the observation. So, too, would be whether a barrier filter such as the Kodak Wratten #12 is used.²

When we attempt to interpret the pattern of staining, the clinical task is to be able to differentiate between these possible mechanisms: surface pooling, uptake by cells, or ingress around cells. It has been found that even normal epithelial cells may be moderately permeable to fluorescein.²

The presence of increased numbers of inflammatory cells in DED has also been documented.³ Chinese researchers found an increased number of Langerhans cells and increased density of leukocytes in a dry eye population (normals = 33, DED = 46). The amount of change observed correlated with disease severity.³ Increased numbers of leukocytes were also detected in a study on midday fogging associated with scleral lens wear.⁴

The pattern of epithelial staining is sometimes a clue to the etiology. Staining that is largely confined to the inferior half of the cornea may indicate exposure keratitis due to an incomplete blink, lagophthalmos, blepharitis, or trichiasis.⁵ Diffuse staining involving the entire cornea may be indicative of the so-called “solution toxicity” in patients wearing soft contact lenses.⁶ However, this remains controversial as a similar pattern has been observed in patients who use extended-wear lenses.⁷ An alternative explanation has been put forth as an innocuous, non-pathological condition referred to as PATH (preservative-associated transient hyperfluorescence).⁸

References

1. Hauswirth SG. When dry eye compromises corneal integrity. Rev Opt. 15 Nov 2017. Available at https://www.reviewofoptometry.com/article/ro1117-when-dry-eye-compromises-corneal-integrity . Accessed June 15, 2022.
2. Morgan PB, Maldonado-Codina C. Corneal staining: Do we really understand what we are seeing? Cont Lens Anterior Eye. 2009 Apr;32:48-54.
3. Lin H, Li W, Dong N, et al. Changes in corneal epithelial layer inflammatory cell is aqueous tear-deficient dry eye. Invest Ophthalmol Vis Sci. 2010 Jan;51:122-128.
4. Postnikoff CK, Pucker AD, Laurent J, Huisingh C, McGwin G, Nichols JJ. Identification of leukocytes associated with midday fogging in post-lens tear film of scleral contact lens wearers. Invest Ophthalmol Vis Sci. 2019 Jan 2;60:226-233.
5. Vislisel J, Karakas S. Punctate epithelial erosions (PEE) in exposure keratopathy. EyeRounds.org . Available at webeye.ophth.uiowa.edu/eyeforum/atlas/pages/Punctate-epithelial-erosions/index.htm# . Accessed June 15, 2022.
6. Carnt N, Jalbert I, Stretton S, Naduvilath T, Papas E. Solution toxicity in soft contact lens daily wear is associated with corneal inflammation. Optom Vis Sci. 2007 Apr;84:309-315.
7. Szczotka-Flynn L, Debanne SM, Cheruvu VK, et al. Predictive factors for corneal infiltrates with continuous wear of silicone hydrogel contact lenses. Arch Ophthalmol. 2007 Apr;125:488-492.
8. Efron N. Putting vital stains in context. Clin Exp Optom. 2013 Jul;96:400-421.

Editor's Note: The image that ran in the print edition of Contact Lens Spectrum was incorrect. The correct image for this column is pictured above.