AQUEOUS DEFICIENCYThe bulk of the precorneal tear film consists of an aqueous component that is produced by the main and accessory lacrimal glands. Continuous production and drainage of the aqueous layer is vital to maintain the corneal and conjunctival epithelium in a moist state, supply nutrients and bacteriostatic agents, and clear the ocular surface by the flushing action of tear movement. However, the aqueous layer can become partially or absolutely deficient, leading to dry eye. Aqueous deficiency can be caused by either a decrease in tear production or as a result of increased tear evaporation.
Patients who present with a decrease in the aqueous component of the tear film comprise the majority of patients with dry eye. The most commonly encountered condition that occurs as a result of aqueous deficiency is keratoconjunctivitis sicca (KCS). KCS can be treated with artificial tears or lubricant eye drops, such as VISMED®.
MUCIN DEFICIENCYMucin is mainly produced by the goblet cells in the conjunctiva and forms a coating over the corneal epithelium that contributes to tear film stability. It also forms an effective lipid trap and plays a primary role in the removal of lipid contamination from the epithelial surface. However, certain conditions [including vitamin A deficiency, ocular pemphigoid, drug reactions (Stevens-Johnson syndrome) and severe burns (chemical or thermal)] can affect the conjunctiva, resulting in a decrease in goblet cells and leading to mucin deficiency. The integrity of the mucin layer is disrupted and the tear film becomes unstable, resulting in the appearance of nonwetted areas on the corneal and conjunctival surfaces.
In the presence of normal aqueous and lipid production and normal lid function, an abnormally rapid tear film break up time (TBUT) of <10 seconds strongly suggests the presence of a deficient mucus layer. In this case, the abnormal break up of the tear film is a direct measure of the functional ability of the mucus layer and reflects the impaired lipid masking and lipid removal activities of this layer.
LIPID ABNORMALITYAlterations in the lipid composition of the precorneal tear film have been associated with chronic blepharitis. Evidence indicates that although tear production is adequate, certain microbes can secrete the enzyme lipase, which hydrolyses Meibomian lipids to free fatty acids. These free fatty acids are highly surface active, spreading so rapidly that they cause instantaneous dry spot formation in the precorneal tear film. A characteristic of intense lipid–mucin interaction is a decrease in the spreading of the tear film, resulting in a rapid TBUT (seen in chronic blepharitis).
Shear forces produced by the moving lids play a vital role in the maintenance of a normal tear film. Compromise of normal lid–globe contact or an abnormality in the blinking process can adversely affect mucus distribution and turnover, resulting in a well-defined area of nonwetting. Localised drying can occur in exposure keratitis, most commonly seen in connection with VII cranial nerve paresis (Bell’s palsy or facial palsy). In addition, extensive conjunctival inflammation, as seen in Stevens-Johnson syndrome, ocular pemphigoid and chemical burns, can severely limit lid movement. In association with mucin and aqueous tear deficiencies, the effects can be damaging.
IMPAIRED LID FUNCTION
In order to have adequate wetting of the corneal surface, it is necessary to have a normal corneal epithelium. Thus, in situations where there is a disruption in the normal structure of the cornea, such as corneal scars, irregularities and conditions such as anaesthetic cornea, it is quite common to have an unstable tear film and localised areas of drying.
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