The role of lipid abnormalities, aqueous and mucus deficiencies in the tear film breakup, and implications for tear substitutes and contact lens tolerance

Abstract

We had earlier proposed a "two-step, double-film" mechanism of tear film rupture, which traces the instability of the tear film in the van der Waals interaction mediated rupture of the thin mucus coating of the corneal epithelium. A transport model is now formulated for investigating the instability of the mucus layer in the presence of naturally occurring solutes of the tear film. It is shown that the normal lipids of the tear film play a dual role in stabilizing the mucus layer: (1) they augment the mucous-aqueous interfacial tension and (2) they induce an interfacial tension driven Marangoni convection. Both of these oppose the growing interfacial perturbations and consequently, the thinning of the mucus layer which is caused by the van der Waals interactions. An increased surface activity of lipids, due to numerous pathological conditions of the eyes, is shown to affect the tear film breakup time (BUT) adversely. The observed deleterious effects of highly surface active ingredients of tear substitutes, clinical stains, and anesthetics on BUT are also explained within the framework of the proposed mechanism. The aqueous tear deficiency which is reflected in the reduced thickness of the tear film, is shown to facilitate a rapid redistribution of solutes and thus undermines the stabilizing effect of the Marangoni convection. A marginally healthy eye may thus develop dry eye syndromes because of the aqueous tear deficiency. The proposed mechanism is in agreement with clinical observations of the factors causing the dry eyes and numerous other experimental and clinical findings related to the phenomenon of tear film rupture. The role of tear substitutes in prolonging the time of rupture as well as the implications of the present mechanism for the formulation of tear substitutes are delineated. The factors affecting the contact lens tolerance due to the altered physiology of the tear film are discussed. A particular emphasis is, however, placed on the possible adhesion of the contact lens to the cornea. Finally, it is emphasized that the clinical measurements of BUT are an overall outward manifestation of several factors discussed above and their synergisms thereof.