Tears and Contact Lenses

Tear film structure, origin and functions

The tear film ( Fig. 5.1 ) is a carefully ordered structure with a thin layer of lipid on the surface and a thicker aqueous-mucin phase beneath which increases in mucin concentration towards the epithelial cell layer of the cornea. Conferring hydrophilicity to the naturally hydrophobic corneal surface is the thin, innermost layer of membrane-bound mucins described as glycocalyx ( ).

The tear lipid layer (or meibum) is in the order of 50–100 nm thick. It arises mainly from the meibomian glands embedded within the eyelid, with a smaller contribution from the eyelid glands of Moll and Zeis ( , ). Meibum contains both polar and nonpolar components that align to form the duplex structure of the lipid layer: a thin polar layer interfacing with the aqueous layer and a thicker, nonpolar layer blanketing the upper surface exposed to the air. The primary function of the lipid layer is to retard evaporation of the underlying tear fluid, but it also has a role in lowering the surface tension of the tears and in preventing tear spillage over the lid margins ( ).

The lacrimal gland is the main source of the aqueous fluid, with minor contributions from the accessory lacrimal glands of Krause and Wolfring and from epithelial cell secretions ( ). The aqueous component forms the bulk of the tear film ( ) and helps to nurture the avascular cornea by transferring oxygen and nutrients as well as conveying chemical signals between envelop ( ). The electrolytes contained within the aqueous fluid determine its osmolarity as well as help to stabilise tear pH and maintain epithelial integrity. The aqueous tears further defend the ocular surface through their antimicrobial and antioxidant constituents, and they contain growth factors that are critical to ocular surface maintenance and repair ( ).

Soluble, gel-forming mucins, produced by the goblet cells of the conjunctiva, increase in concentration towards the base of the aqueous tear layer ( ). These mucins help lubricate the ocular surface, promoting a smooth and intact surface to facilitate the blinking action of the eyelids. They further protect the corneal cells by encasing debris on the ocular surface for safe removal at the caruncle, via blinking ( ). Supporting this aqueous-mucin gel matrix are transmembrane mucins, which are anchored to the epithelial cells of the cornea and conjunctiva and contribute to the glycocalyx. As well as promoting hydrophilicity, these mucins further protect the ocular surface.

Blinking spreads the tear film, replenishes its components and reforms its structure. After a blink, the compressed lipid layer is stretched across the exposed interpalpebral area as the eye opens, drawing beneath it the replenished aqueous layer ( ). Between blinks, the tear film thins and destabilises. Altered interfacial tensions cause contamination between the layers and the formation of dry spots within the film, evaluated clinically as tear film breakup. Regular and complete blinks are required to avoid such destabilisation. For the ocular surface to be protected, the period of tear film stability must exceed the interblink interval ( ).

The tear film in the non–contact lens–wearing eye

The ocular surface and tear film are closely interdependent, and an imbalance in one or the other can result in tear film instability and trigger the cycle of hyperosmolarity, inflammation and further loss of tear film integrity observed in dry eye.

Normal tear film thickness over the central cornea is approximately 3 µm, and the rate of tear turnover, corresponding primarily to replenishment of the aqueous tear component, is approximately 15.5% per minute ( , ).

Lipid layer grade and tear film stability

Lipid layer thickness can be graded on a six-point scale (see Fig. 5.8 ), according to the pattern visible with interferometry ( ). A normal tear film exhibits at least a closed-meshwork lipid layer pattern. Thinner lipid layers are associated with poor tear film stability ( ). Tear film instability is a core feature of dry eye that occurs not only in the presence of a poor lipid layer, but also from dysfunction of any one of the tear components or the ocular surface itself. Aqueous deficiency, mucin abnormality or excessive evaporation, or any combination of these, can contribute to an unstable tear film.

Tear film evaporation and hyperosmolarity

Disruption of the tear film structure, reflected in a loss of tear film stability, leads to increased evaporation of the tears, triggering tear film hyperosmolarity. Aqueous deficiency and excessive evaporation often coexist and are the major aetiological classes of dry eye identified by the TFOS (Tear Film and Ocular Surface Society) Dry Eye Workshop (DEWS Report, 2007 and 2017) (see also Section 9 , Addendum, available at: https://expertconsult.inkling.com/ ).

Hyperosmolarity reflecting a high tear solute concentration is an indicator of tear film homeostatic imbalance. It is considered a core feature in the pathophysiology of dry eye ( , ). The electrolytes sodium, chloride, potassium and bicarbonate are the predominant contributors to tear film osmolarity, while tear film proteins and sugars have little influence ( ).

Tear film biochemical composition

This can be described according to its proteome (proteins and peptides), lipidome (lipids), mucins and glycocalyx, and other components (see also Section 9 , Addendum, available at: https://expertconsult.inkling.com/ ).

Clinical changes

• ▪

  Placing a contact lens within the preocular tear film induces both biophysical and biochemical alterations to the tear film ( ). A contact lens is in the order of 30 times thicker than the tear film and divides the naturally ordered preocular film into the anterior, prelens tear film and the posterior, post-lens tear film, sandwiched between the posterior lens surface and the anterior ocular surface.

• ▪

  Wearing a lens can result in incomplete blinks where the eyelids cover less than two-thirds of the cornea during a blink especially in rigid lens wearers. In soft lens wearers, incomplete blinking causes symptoms of dryness and discomfort, lens deposits and increased corneal fluorescein staining.

• ▪

  The lipid layer of the prelens tear film is adversely affected by contact lens wear. This is attributed to the reduced prelens aqueous layer, which impedes tear film lipid layer spread after a blink ( , , ). The lens may also exhibit areas with poor wettability, which predisposes the lens surface to deposition-impaired optical quality.

• ▪

  Tear film stability, measured noninvasively, has been reported to be useful as a predictor of symptoms ( ).

• ▪

  Tear evaporation rate increases with all lens wear, suggesting that physical disruption to the tear film in the presence of a lens is the primary driver of excessive evaporation, rather than the lens material or fit.

• ▪

  At approximately 2 µm, the prelens tear film is thinner than the preocular tear film by approximately 1 µm ( , ), possibly predisposing the fluid to the more rapid destabilisation described previously. Instilling artificial tears can increase the prelens tear film thickness, but the effect is transient and the post-lens tear film shows minimal fluctuation ( ).

• ▪

  Asymptomatic contact lens wearers have a greater basal tear flow rate than symptomatic wearers, perhaps helping to counteract the loss of tear fluid from the higher tear evaporation rate in contact lens wear ( ).

Biochemical changes

(see Section 9 , Addendum, available at: https://expertconsult.inkling.com/ )

Anterior eye (see Chapter 6 , Chapter 8 , Chapter 15 )

Carry out a general slit-lamp examination and assess parameters using standardised clinical grading scales (e.g. Brien Holden Vision Institute (BHVI) (for further information see https://expertconsult.inkling.com/ ), Efron), including:

• ▪

  Ocular bulbar redness is a common and nonspecific clinical sign that can be associated with several factors, including dryness, exposure, inflammation and infection ( Fig. 5.3 ). The location, pattern and depth of the response can assist with guiding the diagnosis. For example, vasodilation of the blood vessels adjacent to the limbus may be associated with a hypoxic-driven response to contact lens wear or may indicate inflammation within the uveal tissues.

  

• ▪

  Evaluation of the eyelids with regard to:

  • ▪

    hyperaemia ( Fig. 5.4a )

    

  • ▪

    oedema ( Fig. 5.4a )

  • ▪

    thickening ( Fig. 5.4a )

  • ▪

    telangiectasia ( Fig. 5.4a )

  • ▪

    concretions

  • ▪

    keratinsation ( Fig. 5.4b )

  • ▪

    irregularity ( Fig. 5.4c ).

• ▪

  The lashes for signs commonly associated with meibomian gland dysfunction (MGD):

  • ▪

    madarosis ( Fig. 5.4a )

  • ▪

    poliosis

  • ▪

    trichiasis

Blepharitis

Any anterior blepharitis (crusting as shown in Fig. 5.4d ). MGD or anterior blepharitis should preferably be managed before contact lens fitting is attempted. The presence of notching of the inferior eyelid ( Fig. 5.4c ) may be a sign of long-standing meibomian gland disease, with associated gland atrophy. Evert the superior eyelid to check for a conjunctival papillary response (see Chapters 12 & 16 ).

• ▪

  Examine the corneal and conjunctival integrity before instilling diagnostic dyes, and note anomalies such as pingueculae or pterygia. Folds in the bulbar conjunctiva (LIPCOF – see page 110 ) are likely to prevent the formation of a normal tear reservoir and are an indicator of conjunctival dryness.

• ▪

  Assess the overall tear film quality, in particular looking for the presence of frothing or foaming which may be indicative of MGD ( Fig. 5.5 ).

  

Tear compositional integrity can be quantified by measuring tear osmolarity ( Fig. 5.6 ). A value greater than or equal to 316 mOsmol/L provides high predictive accuracy for diagnosing dry eye ( ).

Tear lipid layer

Tear Film Stability

The most common method for assessing tear film stability is tear film break-up time (TBUT). This technique involves instilling a small volume of sodium fluorescein into the eye and observing the integrity of the precorneal tear film by slit-lamp biomicroscopy using cobalt blue illumination, which can be enhanced with a Wratten-12 yellow barrier filter. TBUT is the time, in seconds, between a complete blink and the first dark patch (break) appearing in the film ( ).

TBUT is:

• ▪

  shorter in females than males

• ▪

  shorter in Asians than Caucasians. In Caucasians, a TBUT of less than 10 seconds is considered a marker of tear film instability ( ) but for Asians 7 seconds is adequate ( ).

Measuring TBUT with sodium fluorescein has several limitations:

• ▪

  The method is poorly reproducible.

• ▪

  Instilling fluid into the eye affects tear stability ( ).

• ▪

  Measurement accuracy can be influenced by factors such as the volume and pH of instilled fluid, slit-lamp illumination level and clinician expertise ( ).

These limitations provide rationale for utilising less invasive tear stability measures (see Table 5.1 ). Several techniques for measuring noninvasive tear break-up time NIBUT are available, most of which involve the observation and/or quantification of the integrity of a reflected-grid or videokeratographic mire pattern from the precorneal film ( Fig. 5.7 ) (see Video 5.1 ). Normative values depend on the instrumentation and will not necessarily correlate well with traditional TBUT measures derived using sodium fluorescein ( , ).

Tear stability can be quantified for the prelens tear film to assess lens wettability. Contact lens wear thins the tear lipid layer, leading to a relatively reduced prelens NIBUT ( , ), more rapid tear evaporation ( ) and accelerated tear thinning ( ) compared with no lens wear. The gradual accumulation of surface deposits in rigid lens wear exacerbates the effects of poor prelens wetting and emphasises the need for appropriate lens maintenance and regular lens replacement with this modality.

Impaired tear stability is associated with higher levels of ocular discomfort during contact lens wear, and symptomatic soft lens wearers show significant differences in their prelens tear film kinetics. In a retrospective analysis, symptomatic soft lens wearers were found to have reduced surface coverage of the lens by the tear film during the interblink period and a greater proportion of surface exposure at the time of blink than asymptomatic lens wearers ( ). Evaluating prelens tear film kinetics may be valuable, therefore, for monitoring the efficacy of management strategies (e.g. changes to lens materials and/or contact lens solutions) aimed at supporting the prelens tear film to enhance lens comfort.

Key Point

Evaluating tear stability, as relevant to contact lens wear:

• The level of tear film stability relates to the degree of comfort during contact lens wear.

• Noninvasive measures of tear stability are preferable for examining the tear film in its natural state compared with traditional measures requiring the instillation of sodium fluorescein.

• Automated measurement systems are clinically useful for determining NIBUT; however, diagnostic criteria for tear instability are instrument-specific.

• The wettability of a contact lens in situ can be quantified dynamically using similar techniques to measuring precorneal NIBUT.

Lipid Layer Evaluation

The nature of the tear film's thin layer of lipid adjacent to the different refractive index of the aqueous phase allows visualisation of the oil layer by thin film interferometry for estimation of quality and thickness. Specular reflection of white light from the lipid layer of the tears generates first order coloured interference fringes when the lipid thickness exceeds one-quarter of the wavelength of light. These coloured fringes can sometimes be seen on standard slit-lamp biomicroscopy. However, lipid layer thicknesses in the normal tear film are often less than 100 nm, and so colours are not visible. A meaningful assessment of the lipid layer by interferometry thus requires a wide-field, cold, broad-spectrum light source to allow observation of thinner layers.

Although precise quantification of lipid thickness is most accurately achieved with the use of single-wavelength interferometers ( ), white-light interferometry reveals patterns characteristic of a particular lipid thickness range, which can be classified according to published grading scales ( Fig. 5.8 ) ( ). The following numbered lipid pattern grading scale, based on the ordinal Guillon scale ( , ), is helpful in the clinical setting for assessment and review:

Open Meshwork (Grade 1).

This describes an extremely thin lipid layer. By virtue of the lipid thickening when it is compressed between the eyelid margins during a blink, this pattern tends to be visible only by the postblink movement. When the eye is fully open and the lipid is maximally stretched over the tear film surface, it is often no longer visible.

Closed Meshwork (Grade 2).

In clinical appearance, this pattern has been likened to marble, fish scales or loosely stretched knitting ( Fig. 5.8a ). It is similar in appearance to the open meshwork pattern, except that because of its greater thickness, the closed meshwork pattern remains stable and clearly visible between blinks when the eye is fully open.

Wave (Grade 3).

This is the most commonly observed pattern in the non–lens-wearing eye ( Fig. 5.8b ) (see Video 5.2 ). It is visible as parallel streaks or waves flowing across the tear film surface signifying increasing thickness of the lipid layer. The waves can flow either horizontally or vertically (i.e. parallel or perpendicular to the lid margins).

Amorphous (Grade 4).

This highly reflective layer has a stable, whitish, even appearance indicating a good-quality, thick lipid layer, which is considered ideal for contact lens wear ( Fig. 5.8c ). A tip to help avoid confusion when differentiating between an amorphous or absent lipid pattern, since both lack discernible features, is to ask the patient to partially close his or her eyes. Compression of the lipid layer between the lid margins will induce a coloured fringe appearance in the case of a thicker amorphous lipid pattern but not in the case of a thin or absent pattern.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here