Tear-film instability is widely believed to be a signature of eye health. When an interblink is prolonged, randomly distributed ruptures occur in the tear film. "Black spots" and/or "black streaks" appear in 15 to 40 s for normal individuals. For people who suffer from dry eye, tear-film breakup time (BUT) is typically less than a few seconds. To date, however, there is no satisfactory quantitative explanation for the origin of tear rupture. Recently, it was proposed that tear-film breakup is related to locally high evaporative thinning. A spatial variation in the thickness of the tear-film lipid layer (TFLL) may lead to locally elevated evaporation and subsequent tear-film breakup. We examine the local-evaporation-driven tear-film-rupture hypothesis in a one-dimensional (1-D) model for the evolution of a thin aqueous tear film overriding the cornea subject to locally elevated evaporation at its anterior surface and osmotic water influx at its posterior surface. Evaporation rate depends on mass transfer both through the coating lipid layer and through ambient air. We establish that evaporation-driven tear-film breakup can occur under normal conditions but only for higher aqueous evaporation rates. Predicted roles of environmental conditions, such as wind speed and relative humidity, on tear-film stability agree with clinical observations. More importantly, locally elevated evaporation leads to hyperosmolar spots in the tear film and, hence, vulnerability to epithelial irritation. In addition to evaporation rate, tear-film instability depends on the strength of healing flow from the neighboring region outside the breakup region, which is determined by the surface tension at the tear-film surface and by the repulsive thin-film disjoining pressure. This study provides a physically consistent and quantitative explanation for the formation of black streaks and spots in the human tear film during an interblink.

Purpose

We developed an in vitro model-blink cell that reproduces the mechanism of in vivo fouling of soft contact lenses. In the model-blink cell, model tear lipid directly contacts the lens surface after forced aqueous rupture, mirroring the pre-lens tear-film breakup during interblink.

Methods

Soft contact lenses are attached to a Teflon holder and immersed in artificial tear solution with protein, salts, and mucins. Artificial tear-lipid solution is spread over the air/tear interface as a duplex lipid layer. The aqueous tear film is periodically ruptured and reformed by withdrawing and reinjecting tear solution into the cell, mimicking the blink-rupture process. Fouled deposits appear on the lenses after cycling, and their compositions and spatial distributions are subsequently analyzed by optical microscopy, laser ablation electrospray ionization mass spectrometry, and two-photon fluorescence confocal scanning laser microscopy.

Results

Discrete deposit (white) spots with an average size of 20 to 300 μm are observed on the studied lenses, confirming what is seen in vivo and validating the in vitro model-blink cell. Targeted lipids (cholesterol) and proteins (albumin from bovine serum) are identified in the discrete surface deposits. Both lipid and protein occur simultaneously in the surface deposits and overlap with the white spots observed by optical microscopy. Additionally, lipid and protein penetrate into the bulk of tested silicone-hydrogel lenses, likely attributed to the bicontinuous microstructure of oleophilic silicone and hydrophilic polymer phases of the lens.

Conclusions

In vitro spoilation of soft contact lenses is successfully achieved by the model-blink cell confirming the tear rupture/deposition mechanism of lens fouling. The model-blink cell provides a reliable laboratory tool for screening new antifouling lens materials, surface coatings, and care solutions.

Hyperosmotic tear stimulates human corneal nerve endings, activates ocular immune response, and elicits dry-eye symptoms. A soft contact lens (SCL) covers the cornea preventing it from experiencing direct tear evaporation and the resulting blink-periodic salinity increases. For the cornea to experience hyperosmolarity due to tear evaporation, salt must transport across the SCL to the post-lens tear film (PoLTF) bathing the cornea. Consequently, limited salt transport across a SCL potentially protects the ocular surface from hyperosmotic tear. In addition, despite lens-wear discomfort sharing common sensations to dry eye, no correlation is available between measured tear hyperosmolarity and SCL-wear discomfort. Lack of documentation is likely because clinical measurements of tear osmolarity during lens wear do not interrogate the tear osmolarity of the PoLTF that actually overlays the cornea. Rather, tear osmolarity is clinically measured in the tear meniscus. For the first time, we mathematically quantify tear osmolarity in the PoLTF and show that it differs significantly from the clinically measured tear-meniscus osmolarity. We show further that aqueous-deficient dry eye and evaporative dry eye both exacerbate the hyperosmolarity of the PoLTF. Nevertheless, depending on lens salt-transport properties (i.e., diffusivity, partition coefficient, and thickness), a SCL can indeed protect against corneal hyperosmolarity by reducing PoLTF salinity to below that of the ocular surface during no-lens wear. Importantly, PoLTF osmolarity for dry-eye patients can be reduced to that of normal eyes with no-lens wear provided that the lens exhibits a low lens-salt diffusivity. Infrequent blinking increases PoLTF osmolarity consistent with lens-wear discomfort. Judicious design of SCL material salt-transport properties can ameliorate corneal hyperosmolarity. Our results confirm the importance of PoLTF osmolarity during SCL wear and indicate a possible relation between PoLTF osmolarity and contact-lens discomfort.