(271c) Interfacial Phenomena Undergird Human Eye Health

A healthy human eye relies on the integrity of the tear film to protect the cornea. Interfacial phenomena govern the behavior of the tear-film system. Capillary hydrodynamics sets the thickness of the deposited film (at about 3 µm) and provides the smoothness necessary for precise vision. Meniscus-driven capillary suction pinches film extremities forming McDonald-Brubaker lines that prevent gravity-driven slough off. Spreading of a 100-nm lipid-layer of meibum over the tear film significantly slows evaporation rates that otherwise would consume the entire the tear layer during an interblink. Without capillarity, the human eye cannot function properly. We show here, however, that capillarity also causes dry-eye disease: a burny, itchy, scratchy feeling of dryness and discomfort. Dry eye infects up to 30 % of the global population. It is especially prevalent in the elderly and women, and in arid, windy climates.

The etiology of dry eye arises from clinical observation that during an interblink randomly distributed ruptures occur in the tear film. Under sodium-fluorescein instillation, â??black spotsâ? and/or â??black streaksâ? appear in less than a few seconds for people who suffer from dry eye. Rapid tear breakup strongly correlates to dry-eye syndrome. In spite of decades of effort, however, there is no physically consistent explanation for how a 3-µm aqueous film on a water-wetting corneal surface breaks up within a few seconds, nor is there an explanation for how such ruptures give rise to dry-eye symptoms.

We propose local evaporative-driven tear rupture. Our proposal relies on interferometric observations that the 100-nm the meibum coating film is unstable, in agreement with in-vitro experiments on duplex oil films spread on water. Once the covering lipid-film ruptures, underlying tear evaporates at much higher rate (near that of pure water). Increased evaporation drives a deepening hole in the tear film relative to surrounding lipid-covered domains. The growing hole is suppressed by curvature-driven healing flow and by osmotic-suction from the cornea due to a local salinity increase. Rupture occurs only when the locally high evaporative flux outweighs the two healing flows. Our one-dimensional stability analysis is in excellent agreement with clinical observations on times for breakup and on environmental roles of wind speed and relative humidity. New in-vivo measurements of transient infrared ocular surface temperature along with transient tear breakup area confirm faster evaporation rates in expanding tear-rupture holes.

Connection of tear rupture to dry-eye syndrome is the calculated large increases in salinity underneath the deepening rupture holes. Evaporative-driven tear breakup leads to significant increased salinities at the bottom of the rupture spot (or streak) that we coin salinity â??hot spotsâ?. Hyperosmolarity causes eye pain and epithelial cell damage. A tear film peppered with salinity hot spots activates corneal afferent nerve receptors (cold) causing pain sensation and eventually dry eye.

Principles of capillarity are integral to functioning of the human eye and can be applied to understand and hopefully ameliorate dry-eye syndrome.