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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.

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Ophthalmic drug delivery through contact lenses increases bioavailability and reduces systemic drug uptake.

Transport of surface active anesthetic drugs through silicone hydrogel contact lenses containing nanosized vitamin E aggregates is explored for achieving extended anesthetics delivery. Commercial silicone hydrogel contact lenses release most ophthalmic drugs including local anesthetics for only a few hours, which is not adequate. Here we focus on creating dispersion of highly hydrophobic vitamin E aggregates in the lenses as barriers for drug diffusion for increasing the release durations. This approach has been shown previously to be successful in extending the release durations for some common hydrophilic ophthalmic drugs. The topical anesthetic drugs considered here (lidocaine, bupivacaine, and tetracaine) are hydrophilic at physiologic pH due to the charge, and so these cannot partition into the vitamin E barriers. However, these surface active drug molecules adsorb on the surface of the vitamin E barriers and diffuse along the surface, leading to only a small decrease in the effective diffusivity compared to non-surface-active hydrophilic drugs. The drug adsorption can be described by the Langmuir isotherm, and measurements of surface coverage of the drugs on the vitamin E provide an estimate of the available surface area of vitamin E, which can then be utilized to estimate the size of the aggregates. A diffusion controlled transport model that includes surface diffusion along the vitamin E aggregates and diffusion in the gel fit the transport data well. In conclusion, the vitamin E loaded silicone contact lens can provide continuous anesthetics release for about 1-7 days, depending on the method of drug loading in the lenses, and thus could be very useful for postoperative pain control after corneal surgery such as the photorefractive keratectomy (PRK) procedure for vision correction.

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