Abstract
PurposeTo determine whether localized hyperosmotic spikes on the pre-lens tear film (PrLTF) due to tear break up results in hyperosmotic spikes on the ocular surface during soft-contact-lens (SCL) wear and whether wear of SCLs can protect the cornea against PrLTF osmotic spikes. MethodsTwo-dimensional transient diffusion of salt was incorporated into a computationally designed SCL, post-lens tear film (PoLTF), and ocular surface and solved numerically. Time-dependent localized hyperosmolarity spikes were introduced at the anterior surface of the SCL corresponding to those generated in the PrLTF. Salt spikes were followed in time until spikes penetrate through the lens into the PoLTF. Lens-salt diffusivities (Ds) were varied to assess their importance on salt migration from the PrLTF to the ocular surface. SCL and PoLTF initial conditions and the lens anterior-surface boundary condition were varied depending on the value of Ds and on dry-eye symptomatology. Determined corneal surface osmolarities were translated into clinical pain scores. ResultsFor Ds above about 10-7cm2/s, it takes around 5–10 s for the PrLTF hyperosmotic break-up spikes to diffuse across the SCL and reach the corneal surface. Even if localized hyperosmotic spikes penetrate to the ocular surface, salt concentrations there are much lower than those in the progenitor PrLTF spikes. For Ds less than 10-7cm2/s, the SCL protects the cornea from hyperosmotic spikes for both normal and dry eyes. When localized corneal hyperosmolarity is converted into transient pain scores, pain thresholds are significantly lower than those for no-lens wear. ConclusionsA cornea can be protected from localized PrLTF hyperosmolarity spikes with SCL wear. With regular blinking (e.g., less than 10 s), SCL wear shields the cornea from significant hyperosmotic pain. Decreasing Ds increases that protection. Low-Ds soft contact lenses can protect against hyperosmotic spikes and discomfort even during infrequent blinking (e.g., > 10 s).
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