Blinking

CLs elicit reflex blinking during lens insertion, removal and other instances of manual manipulation. Also, as a result of a reflex blink, CLs may mislocate or become dislodged from the eye. Both soft lens wear and rigid lens wear cause the spontaneous blink rate to increase ( ). In rigid lens wear, this change may be more related to reflex blinking rather than spontaneous blinking; that is, the increased blink rate may be a result of continual irritation caused by the lens edge buffeting against the lid margin. Such alterations to blink rate are not thought to be permanent.

CLs can affect the pattern of blinking. A decrease in the frequency of occurrence of long-duration interblink periods occurs in association with rigid lens wear, but not soft lens wear. Neither rigid nor soft lens wear alters the proportion of complete, incomplete, twitch and forced blinks. Infrequent or incomplete blinking with CLs ( Fig. 38.1 ) can cause a number of problems, including lens surface drying and deposition, epithelial desiccation, postlens tear stagnation, hypoxia and hypercapnia and 3 and 9 o’clock staining. Faults in lens design and fitting can interfere with proper blink-mediated lid–lens interaction. Fewer complete eyeblinks, more incomplete eyeblinks and more eye-blink attempts were observed in rigid lens wearers with 3 and 9 o’clock staining compared with those with minimal staining and nonwearers ( ).

Incomplete blink in a soft lens wearer.

(Courtesy Hilmar Bussaker, Bausch & Lomb Slide Library.)

There are essentially two options when faced with a clinical problem relating to nonpathological disorders of spontaneous blinking activity associated with CL wear, such as infrequent and/or infrequent blinking. These options are to train patients to modify their blinking activity ( ) and/or to alter the lens type or lens fit.

Practitioners should always be alert to the possibility that apparent anomalies in the type or pattern or blinking activity in a CL wearer may be attributable to unrelated disease states. Interruptions to the neural input and/or muscular systems of the eyelids can adversely affect normal spontaneous blinking activity. For example, patients with Parkinson’s disease exhibit a low blink rate. Increased mechanical resistance to eyelid movement, as in Graves’ disease, can also reduce blink frequency. Local pathology of the eyelids, such as ptosis, chalazia and carcinomas, can alter eyelid function and movement and hence interfere with normal blinking activity. It is therefore essential to rule out the possibility of unrelated pathology before ascribing blinking dysfunction to CL wear.

Ptosis

The classical appearance of ptosis is of a narrowing of the palpebral fissure and a relatively large gap between the upper-lid margin and the skin fold at the top of the eyelid ( Fig. 38.2 ). measured the palpebral aperture size to be 10.10 ± 1.11 mm in nonwearers and 9.76 ± 0.99 mm in rigid lens wearers; it was unaltered in soft lens wearers. According to , clinically significant ptosis occurs when the distance between the centre of the pupil and the lower margin of the upper lid is less than 2.8 mm. Using this criterion, CL-induced ptosis (CLIP) occurs in about 10% of rigid lens wearers ( ), although suggest that long-term rigid CL wear does not lead to acquired blepharoptosis in Chinese eyes. The ptosis takes 4–6 weeks to develop fully and is generally noticed by patients in advanced cases. There are no associated signs or symptoms.

Unilateral right-eye ptosis induced by the wearing of a rigid lens in the right eye for 4 weeks on an extended-wear basis; the left eye wore a soft lens. Note that the gap between the skin fold (just beneath the eyebrows) and the upper-lid margin is greater in the right eye than the left.

(Courtesy Desmond Fonn, Bausch & Lomb Slide Library.)

A number of mechanisms have been advanced as possible causes of CLIP. Those involving some form of dysfunction of the aponeurosis include forced-lid repeated squeezing and lateral eyelid stretching during lens removal, rigid lens displacement of the tarsus and blink-induced eye rubbing ( ). Nonaponeurogenic causes of CLIP include lens-induced lid oedema, blepharospasm and papillary conjunctivitis. suggest that CLIP is often attributable to fibrosis in Müller muscle.

To differentiate between these possible causes, patients demonstrating CLIP should be required to cease lens wear for at least 1 month (to detect any trends towards recovery) and perhaps as long as 3 months (to demonstrate complete resolution). If the CLIP partially or completely resolves after ceasing lens wear for 1 month, then the cause is lid oedema and/or involuntary blepharospasm, and the patient may need to be refitted with soft lenses (which do not induce ptosis). The eyelids should also be inverted to determine whether papillary conjunctivitis is involved and, if so, whether appropriate action should be taken to alleviate the condition. If the ptosis persists after resolution of the papillary conjunctivitis, or after ceasing lens wear for 1 month, then the cause is most likely damage to the aponeurosis or Müller muscle, whereby surgical correction is the preferred option. Management strategies available to patients with severe CLIP who do not wish to undergo lid surgery include being fitted with a ‘ptosis crutch’ ( Fig. 38.3 ).

Scleral lens with ‘ptosis crutch’ in the form of two lugs and a shelf.

(Courtesy Frank Pettigrew.)

The prognosis for recovery from aponeurogenic CLIP is poor; the condition can be reversed only by surgical correction or by other management options as described above. The prognosis for recovery from nonaponeurogenic CLIP is good. If the cause of ptosis is papillary conjunctivitis, the time course of resolution of the ptosis will parallel the time course of recovery of the papillary conjunctivitis.

If a CL wearer presents with ptosis, the numerous other possible causes of this condition must be considered so that the appropriate course of management can be adopted.

Meibomian Gland Dysfunction

Meibomian gland dysfunction (MGD) is defined as a chronic, diffuse abnormality of the meibomian glands, commonly characterized by terminal duct obstruction and/or qualitative/quantitative changes in the glandular secretion. It may result in alteration of the tear film, symptoms of eye irritation, clinically apparent inflammation and ocular surface disease ( ).

MGD is classified into two major categories based on meibomian gland secretion: low-delivery states and high-delivery states. Low-delivery states are further classified as hyposecretory or obstructive, with cicatricial and noncicatricial subcategories. Hyposecretory MGD describes the condition of decreased meibum delivery due to abnormalities in meibomian glands without remarkable obstruction. Obstructive MGD is due to terminal duct obstruction. In the cicatricial form, the duct orifices are dragged posteriorly into the mucosa, whereas these orifices remain in their normal positions in noncicatricial MGD. High-delivery, hypersecretory MGD is characterized by the release of a large volume of lipid at the lid margin that becomes visible on application of pressure onto the tarsus during examination. Overall, MGD can lead to alterations of the tear film, symptoms of eye irritation, inflammation and dry eye ( ).

Tear film lipids are essential for ease and comfort in CL wear, but also form deposits on lenses. It is possible that CL wear itself disrupts the meibomian glands and/or lipid layer and leads to tear film evaporation and ocular surface discomfort.

The oily secretion from the normal meibomian gland is generally clear. One diagnostic feature of CL-associated MGD (CL-MGD) is a change in the appearance of the clear oil expressed from healthy meibomian glands to a cloudy, creamy-yellow appearance ( Fig. 38.4 ). Frothing or foaming of the lower tear meniscus is sometimes observed in CL-MGD, especially towards the outer canthus ( Fig. 38.5 ). This appearance is accompanied by symptoms of smeary vision, greasy lenses, dry eyes and reduced tolerance to lens wear ( ). In severe cases where the meibomian orifices are blocked, there may be an absence of gland secretion. Long-standing cases of CL-MGD may be associated with additional signs such as irregularity, distortion and thickening of eyelid margins, slight distension of glands, gland drop-out, mild-to-moderate papillary hypertrophy, vascular changes and chronic chalazia. The prevalence of CL-MGD is unrelated to gender but increases with age.

Inspissated meibomian gland secretion in the lower lid of a female patient wearing rigid lenses.

(Courtesy Lyndon Jones, Bausch & Lomb Slide Library.)

Frothing in the tear film due to meibomian gland dysfunction.

(Courtesy Lourdes Llobet, Bausch & Lomb Slide Library.)

Associated signs of CL-MGD include all those that arise from clinical diagnostic procedures that are designed to indicate the integrity or otherwise of the lipid layer. Specifically, patients suffering from CL-MGD may display a reduced tear break-up time (measured either with fluorescein or noninvasively). Examination of the tear layer in specular reflection using a Tearscope may reveal a contaminated lipid pattern, which is exacerbated by the use of cosmetic eye make-up. Symptoms of blurred or greasy vision can probably be attributed to adhesion of waxy dysfunctional meibomian oils to the surface of the CL; this can lead to lens surface drying, lens dehydration and sensations of dryness.

There is probably no single cause of CL-MGD; proposed aetiological factors include microtrauma from high modulus silicone hydrogel lenses ( ), excess eye rubbing causing chronic damage to meibomian glands and papillary conjunctivitis. From a tissue pathology standpoint, obstructive MGD is characterized by increased keratinization of the epithelial walls of meibomian gland ducts. As might be expected, therefore this condition is often observed in combination with seborrhoeic dermatitis and acne rosacea. This leads to the formation of keratinized epithelial plugs that create a physical blockage in meibomian ducts, which in turn restricts or prevents the outflow of meibomian oils. have shown that CL wear is associated with a decrease in the number of functional meibomian glands and that this decrease is proportional to the duration of lens wear.

Although it may not be possible to treat the underlying cause of CL-MGD symptomatic relief can be provided by adopting one or more of the following procedures, all of which should be undertaken with CLs removed:

• •
  

  application of warm compresses

  
  
• •
  

  lid scrubs

  
  
• •
  

  mechanical expression

  
  
• •
  

  prescription of antibiotics

  
  
• •
  

  use of artificial tears

  
  
• •
  

  omega-3 dietary supplements

  
  
• •
  

  use of surfactant lens cleaners

By adopting these procedures, CL-MGD can be kept under good control and adverse symptoms minimized ( ).

Lid Wiper Epitheliopathy

The lid wiper is a thin strip of tissue near the lid margin that is in contact with the ocular surface or anterior lens surface (where CLs are worn). It is responsible for spreading tears across the ocular surface during blinking ( ). In the upper eyelid, the lid wiper extends about 0.6 mm from the crest of the sharp posterior (inner) lid border (i.e. the mucocutaneous junction, or line of Marx) to the subtarsal fold superiorly and from the medial upper punctum to the lateral canthus horizontally ( ).

Histologically, the lid wiper is seen as an epithelial elevation comprising stratified epithelium with a conjunctival structure of cuboidal cells, some parakeratinised cells and goblet cells ( ). Lid wiper epitheliopathy denotes staining of the lid wiper after instillation of dyes such as fluorescein, rose bengal or lissamine green. Although advocate the use of a simultaneous combination two dyes to stain the lid wiper, most clinicians and researchers seem to favour the use of lissamine green alone ( ).

Higher rates of lid wiper epitheliopathy have been reported in dry-eye patients and CL wearers; however, published evidence supporting these observations is sometimes conflicting ( ). The primary cause of lid wiper epitheliopathy is thought to be increased friction between the lid wiper and ocular or anterior CL surface due to inadequate lubrication, which could be caused by dry eye and may be exacerbated by factors such as abnormal blinking patterns, poor CL surface lubricity and adverse environmental influences ( ). Lid wiper epitheliopathy may be associated with subclinical inflammation ( ).

The optimal procedure for observing lid wiper epitheliopathy is to use a paper strip impregnated with 1 mg lissamine green. The paper strip is moistened with 50 μL of saline and applied to the eye. This procedure is repeated 1 minute later. The eyelid is everted 3 minutes after the second instillation to visualize the lid wiper. It is important to differentiate between normal staining of the line of Marx – a 0.1-mm wide strip that constitutes the region of the mucocutaneous junction of the upper and lower lids that is essentially located along the distal margin of the lid wiper ( Fig. 38.6 ) – and lid wiper epitheliopathy ( Fig. 38.7 ). The line of Marx is visible with lissamine green staining in upgaze without lid eversion, whereas observation of the lid wiper requires lid eversion.

Normal appearance of the mucocutaneous junction (line of Marx) observed at the lid margin as a fine green line following instillation of lissamine green.

(Image courtesy Maria Navascues Cornago.)

Lid wiper epitheliopathy revealed by lissamine green staining in the everted eyelid. A broad band of staining extends below the clearly visible line of Marx. Staining is apparent across the full lateral width of the lid wiper.

(Image courtesy Maria Navascues Cornago.)

Management of severe lid wiper epitheliopathy is indicated if the patient is experiencing moderate to severe discomfort. The management strategy adopted will depend on the cause of the condition, which is not always obvious. Treatment options that have been advocated include the following:

• •
  

  rebamipide – this is an amino acid derivative of 2-(1 H )-quinolinone and is used for mucosal protection, healing of gastroduodenal ulcers and treatment of gastritis. Administration of topical rebamipide increases secretion of mucins from goblet cells and improves the ocular surface in the ‘short break-up time’ type of dry eye

  
  
• •
  

  corticosteroids

  
  
• •
  

  lubricant eye drops

  
  
• •
  

  basic fibroblast growth factor

  
  
• •
  

  LipiFlow Thermal Pulsation System

  
  
• •
  

  punctal plugs

  
  
• •
  

  fit CLs of high surface lubricity

  
  
• •
  

  alter lens wearing modalities – such as reducing lens wearing time, increasing lens replacement frequency and changing lens material properties (modulus of elasticity, silicone/water content, surface-active agents or packaging wetting agents)

  
  
• •
  

  improve blinking behaviour

Eyelash Disorders

Disorders of the eyelashes (cilia), and of associated structures at the base of the eyelashes such as the eyelash follicles, glands of Zeis and Moll and skin of the lid margin, have implications with respect to CL wear. An external hordeolum (stye) presents as a discrete, tender swelling of the anterior lid margin; specifically, it is an inflammation of the tissue lining the lash follicle and/or an associated gland of Zeis or Moll. CLs may add to the discomfort due to the mechanical effect of the lens, and patients may prefer to cease lens wear during the acute phase of the formation of a stye.

Blepharitis is classified as being either anterior or posterior. Posterior blepharitis is a disorder of the meibomian glands; this was considered earlier. Anterior blepharitis is directly related to infections of the base of the eyelashes and manifests in two forms – staphylococcal and seborrhoeic. Staphylococcal anterior blepharitis is caused by a chronic staphylococcal infection of the eyelash follicles. The lid margins are covered in shiny brittle scales ( Fig. 38.8 ), and patients may complain of burning, dryness, itching, foreign-body sensations and mild photophobia. Management strategies include antibiotic ointment, promoting lid hygiene ( ), application of weak topical steroids and artificial tears. Seborrhoeic anterior blepharitis is due to a disorder of the glands of Zeis and Moll. The signs and symptoms are similar but less severe than for staphylococcal anterior blepharitis.

Staphylococcal anterior blepharitis.

(Courtesy Debbie Jones, Bausch & Lomb Slide Library.)

CL wear is generally contraindicated during an acute phase of anterior blepharitis, especially if the cornea is compromised. Attention to lens cleaning is critical to prevent continued recontamination of the eye. Daily disposable CLs will eliminate the problem of recontamination by CLs.

Infestation of the eyelashes by mites or lice can lead to signs and symptoms that closely resemble marginal blepharitis. Typical symptoms include pruritus, burning, crusting, itching, swelling of the lid margins and loss and easy removal of lashes. The itching often parallels the 10-day mite reproductive cycle.

The pubic or ‘crab’ louse ( Phthirus pubis ) has two pairs of strong grasping claws on the central and hind legs, allowing it to hold on to eyelashes with considerable tenacity. Crab louse infestation (phthiriasis) is considered to be a venereal disease because it is passed on by sexual contact, although infestation from contaminated bedding and towels is another possible mode of transfer.

Signs of phthiriasis include pruritus of the lid margins, blepharitis, marked conjunctival injection, madarosis and the presence of lice as well as oval, greyish-white nit shells attached to the base of lashes ( Fig. 38.9 ). Additional signs include preauricular lymphadenopathy and secondary infection along the lid margins at the site of lice bites. The most predominant symptom is intense itching. The initial course of action is to attempt to remove as many mites and mite eggs as possible. Patients should be advised to engage in vigorous lid scrubbing twice daily using commercially available preparations. In general, CL wearers presenting with parasitic infestation of the eyelids should be treated in the same way as similarly infested nonlens wearers ( ).

A nearly transparent crab louse can be seen at the root of the lashes, surrounded by nits encapsulated in shells and some empty shells.

(Courtesy Patrick Caroline, Bausch & Lomb Slide Library.)

Dry Eye

Of all the symptoms experienced by CL wearers, that of ‘dryness’ is reported most frequently ( ); about half of all wearers have symptoms of dryness and discomfort ( ). A major difficulty in assessing the symptom of ‘dryness’ is that there may be many stimuli that elicit this sensation – that is, it cannot be assumed that the cause of a patient symptom of ‘dryness’ is necessarily due to the eye being dry. Because there are no specific ‘dryness receptors’ in human tissue, ocular dryness must be a response to specific coding of afferent neural inputs. Aside from an actual dry eye, reports of ‘dryness’ may arise from the neural misinterpretation of stimuli that are unrelated to dry eye, such as vasodilation induced by mechanical irritation of ocular tissues by deposits on the lens surface. Thus the condition of ‘dry eye’ may be related to a broad spectrum of tear film abnormalities in addition to a reduced tear volume.

A prudent initial approach in dealing with a tentative diagnosis of CL-induced dry eye is to apply a comprehensive questionnaire that draws in other systemic correlates of dryness, such as dryness of other mucous membranes of the body, use of medications, effect of different challenging environments and times when dryness is noted. Such questionnaires can help identify a true dry-eye situation in prospective or current CL wearers and thus form a clinical rationale for more detailed assessment.

The most fundamental test that a clinician can apply when investigating dry eye is to observe the tear film and adjacent ocular structures using the slit-lamp biomicroscope. The overall integrity of the tears during lens wear can be assessed by observing the general flow of tears over the lens surface following a blink, as indicated by the movement of tear debris. A sluggish movement may indicate an aqueous-deficient, mucus-rich and/or lipid-rich tear film and the amount of debris provides an indication of the level of contamination of the tears – for example from overuse of cosmetics. A sluggish and/or contaminated tear film is potentially problematic and could result in increased deposit formation, intermittent blurred vision and symptoms of dryness. Incomplete blinking in soft lens wearers can lead to lens dehydration and consequent epithelial staining of the inferior cornea, corresponding to the position of the palpebral aperture ( Fig. 38.10 ).

Inferior desiccation staining in a patient wearing soft lenses and suffering from dry-eye symptoms.

(Courtesy Michael Hare.)

The volume of tears in prospective and current CL wearers can be assessed by observing the height of the lower lacrimal tear prism. found that measurements of tear meniscus radius of curvature and height ( Fig. 38.11 ) correlated well with results of the cotton thread test, noninvasive tear break-up time and ocular-surface-staining scores, demonstrating the value of such an assessment in diagnosing CL-associated dry eye. Tear volumes in dry-eye symptomatic wearers are lower than in asymptomatic wearers, resulting in the sensation of dryness ( ). A wide-field, cold cathode light source, which is available as a hand-held instrument known as a Tearscope, can be used to assess tear quality during lens wear.

Healthy lower lacrimal tear prism, stained with fluorescein.

(Courtesy Rolf Haberer, Bausch & Lomb Slide Library.)

Most of the strategies that are applied to alleviating signs and symptoms of dry eye of the nonlens-wearing eye can also be applied to the eye during CL wear. In the first instance, attention should be directed to managing the underlying cause if this is known. For example, alleviating CL-MGD, lid wiper epitheliopathy or papillary conjunctivitis (all of which are dealt with elsewhere in this chapter) may lead to a diminution of dry-eye symptoms.

The characteristics of a CL that is most suited for a patient experiencing dry-eye problems are as follows:

• •
  

  a soft lens – with a highly lubricious (low friction) surface and providing full corneal coverage (although some patients report relief from dry-eye symptoms after changing from a soft to a rigid lens)

  
  
• •
  

  a lens that displays minimal in-eye dehydration – to prevent ocular surface desiccation

  
  
• •
  

  a lens that is replaced frequently – for optimal, deposit-free surface characteristics

Numerous other strategies have been advocated for alleviating dry eye, including avoidance of preservatives in care solutions, avoidance of solutions altogether via the use of 1-day disposable lenses, use of rewetting drops, periodic lens rehydration, use of nutritional supplements, control of evaporation, prevention of excess tear drainage (with punctal plugs), use of tear stimulants, reducing wearing time and ceasing lens wear. suggest that CL-related dry eye can be safely alleviated with intense pulsed light treatment.

Mucin Balls

Approximately 50% of patients who wear silicone hydrogel lenses on an extended-wear basis display a peculiar phenomenon known as mucin balls. These formations can be observed in the postlens tear film as small discrete particles, or ‘plugs’ and are similar in appearance to tear film debris. In some patients, as many as 200 mucin balls can be observed. At high magnification (×40), mucin balls can be seen to be of variable size and to take on a characteristic ‘flattened doughnut’ shape, with a thin circular annulus and broad central depression ( Fig. 38.12 ). They are observed in greater numbers in patients who sleep in silicone hydrogel lenses. Mucin balls are immovable beneath the lens and appear to be stuck to the epithelium. A higher number of mucin balls is associated with a looser lens fit ( ). Mucin balls generally increase in number over the first months of lens wear and remain constant thereafter.

Mucin balls displaying characteristic ‘doughnut’ appearance.

(Courtesy Brian Tompkins.)

Mucin balls cause no discomfort or loss of vision and appear to be of no immediate consequence with respect to ocular health ( ). However, there may be cause for concern in the long term. Confocal microscopy, with magnification of up to 650×, has shown mucin balls can penetrate the full thickness of the epithelium, leading to activation of keratocytes in the underlying anterior stroma ( ). The precorneal mucin layer is also known to be an important defence mechanism against infection, by way of preventing attachment of microorganisms to the corneal surface and facilitating the entrapment and removal of microorganisms in the course of the natural turnover of mucus, whereby the mucus is constantly being aggregated, rolled up and flushed from the eye ( ). Lens-induced mucin ball production may therefore represent a compromise to this important protective mechanism.

Mucin balls are composed primarily of collapsed mucin, as well as some lipid and tear proteins ( ). The mechanism by which mucin balls form beneath the lens may in part be related to a physicochemical phenomenon caused by the plasma-treated surface of some types of silicone hydrogel lenses. Specifically, the lipophilic surface of these lenses establishes a complex interfacial relationship with the tear film, which creates a shearing force that has the effect of rolling up tear mucus into small spheres. The mechanical vehicles facilitating such events may be rapid eye movements during sleep and blink-induced lens movement upon awakening.

The relatively high modulus of silicone hydrogel lenses (compared to hydrogel lenses) may also contribute to the above mechanism ( ). In addition, the more viscous, mucus-rich nature of the closed-eye postlens tear film is probably of aetiological significance in the formation of mucin balls. suggest that daily cleaning of extended-wear lenses can reduce mucin ball formation.

Following lens removal, some mucin balls remain ‘stuck’ to the epithelium and some are washed away with blinking but leave behind pits in the epithelial surface, which fill with tear aqueous. Both the remaining mucin balls and the surface fluid-filled pits stain with fluorescein ( Fig. 38.13 ). When viewed at ×40 magnification, the fluid-filled pits give rise to the optical phenomenon of unreversed illumination, which is due to the fact that they are composed of a material (tear aqueous) of lower refractive index than the surrounding epithelial tissue ( Fig. 38.14 ). This appearance is almost identical to dimple veiling caused by air bubbles trapped beneath rigid lenses. Mucin ball-induced fluid-filled pits can therefore be differentiated from epithelial microcysts, which display reversed illumination. Mucin ball-induced fluid-filled pits will stain heavily with fluorescein and give the appearance of an extensive punctate keratitis, whereas epithelial microcysts do not stain except for a few small spots caused by some microcysts breaking through the epithelial surface.

Mucin balls and fluid-filled pits staining with fluorescein.

(Courtesy Kathy Dumbleton, Bausch & Lomb Slide Library.)

Fluid-filled epithelial pits caused by mucin balls displaying unreversed illumination.

(Courtesy Brian Tompkins.)

Conjunctival Staining

evaluated 50 hydrogel lens wearers and 50 nonlens-wearing control subjects for conjunctival staining and symptoms. They disregarded parallel line patterns, which are attributed to pooling of fluorescein in natural conjunctival folds ( Fig. 38.15 ). It was observed that 98% of all subjects displayed some degree of clinically significant conjunctival staining, but only 12% of the nonwearers versus 62% of the lens wearers exhibited staining greater than grade 1. The symptom of dryness was associated with increased conjunctival staining. reported observing conjunctival staining in 33% of 338 adapted hydrogel CL wearers.

Fluorescein fills natural folds in the conjunctiva.

(Courtesy Bausch & Lomb Slide Library.)

An imprint can be created on the conjunctiva as a result of chafing or physical compression by the edge of a soft lens. Chafing may be due to a lens edge design that causes the edge to ‘dig in’ to the conjunctiva. Defects in the lens edge have also been demonstrated to cause increased conjunctival staining ( ). Fitting a lens with a different edge design and a ‘defect-free’ edge will alleviate this problem.

Compression staining will usually be accompanied by a tight-fitting and/or a decentred lens. This manifests as a broad ring of heavy conjunctival staining corresponding to the lens edge, which is clearly evident following lens removal ( Fig. 38.16 ). Conjunctival vessels distal to the lens edge may be engorged. The patient is usually asymptomatic. This condition can be solved by refitting the patient with a lens of greater back optic zone radius.

Conjunctival staining caused by compression from the edge of a tight-fitting soft lens.

(Courtesy Marc Robboy, Bausch & Lomb Slide Library.)

Instillation of fluorescein in a dry-eye patient may reveal the presence of desiccation staining on the conjunctiva, which manifests as a series of diffuse punctate lesions within the interpalpebral zone. The condition will return to normal soon after removing the lens, but long-term resolution may require a combination of treating the underlying cause of the dry eye and refitting the patient with lenses that will facilitate complete conjunctival wetting.

A conjunctival epithelial flap may be seen in patients wearing silicone hydrogel CLs. These arcuate formations on the conjunctiva are composed of sheets of cells detached from the underlying conjunctiva, which probably form as a result of physical irritation by the edge of lenses of higher modulus ( ). They are seen more often in patients wearing lenses on an extended-wear basis ( ). These flaps are asymptomatic and demonstrate minimal histological changes. The clinical significance of conjunctival epithelial flaps is unclear.

Compromise to the conjunctiva as revealed by fluorescein staining is of concern because of recent demonstrations of morphological changes to the conjunctival epithelium associated with lens wear. These changes include alterations to conjunctival cell shape, nuclear morphology and chromatin condensation ( ), and they are reported to be more prevalent in symptomatic lens wearers ( ). Soft lens wear is also associated with a reduction in goblet cell density ( ); this could lead to reduced mucin production, which in turn could explain and perhaps further exacerbate pre-existing symptoms of dryness.

Lid-Parallel Conjunctival Folds

Lid-parallel conjunctival folds are subclinical folds in the lateral, lower quadrant of the bulbar conjunctiva, parallel to the lower lid margin, which are easily observable with the slit-lamp biomicroscope ( ). This is not an adverse ocular reaction; rather, it is a sign of dry eye, including CL-associated dry eye. Lid-parallel conjunctival folds are assessed at two specific locations where they manifest most clearly – just above the lower lid margins, at points where an imaginary perpendicular line projects from the nasal and temporal extremities of the cornea. LIPCOF appear as one or more linear folds of 3–4 mm in length, which are parallel to the lid margin and generally parallel to each other.

Conjunctival Redness

The clinical presentation of a ‘red eye’ can be one of the most difficult cases to solve owing to the numerous possible causes that are known. This problem may be even more complex in a CL wearer because of the wide variety of causes of red eye. Conjunctival redness in lens wearers is generally asymptomatic, but patients may complain of itchiness, congestion, nonspecific mild irritation or a warm or cold feeling ( Fig. 38.17 ). The existence of pain usually indicates corneal involvement or other tissue pathology (e.g. uveitis or scleritis).

Bulbar conjunctival hyperaemia.

The amount of conjunctival redness induced by CLs is less with silicone hydrogel lenses than with conventional hydrogel lenses. In a 4-week study of patients who had not worn lenses previously, observed that conventional hydrogel lenses caused an increase in conjunctival redness of about 0.3 grading scale units (Efron scale), whereas silicone hydrogel lenses induced no change in redness.

The conjunctiva has a rich plexus of arterioles, which contain a thick layer of smooth muscle that is richly enervated with sympathetic nerve fibres. The smooth muscle, as well as being under central autonomic control, can be influenced by numerous local changes. Vasodilation refers to enlargement in the circumference of a vessel due to relaxation of its smooth-muscle layer, which leads to decreased resistance and increased blood flow through the vessel (active hyperaemia). As blood vessels can be observed directly through the transparent conjunctiva, this leads to an appearance of increased redness (less white sclera is visible).

A CL can have a local mechanical effect on the conjunctiva, resulting in increased redness. As a device that can interfere with normal metabolic processes of the cornea and conjunctiva and is used in association with various solutions, a CL can affect the level of conjunctival redness via a local chemical or toxic effect ( Fig. 38.18 ).

General bulbar conjunctival redness, limbal redness and inferior limbal haemorrhages. Adverse reaction to an experimental disinfecting solution in a 22-year-old female soft lens wearer.

(Courtesy Charline Gauthier, Bausch & Lomb Slide Library.)

Local infection and inflammation can cause eye redness. Accordingly, treatment options fall into four broad categories:

• 1.
  

  alterations to the type, design and modality of lens wear

  
  
• 2.
  

  alterations to care systems

  
  
• 3.
  

  improving ocular hygiene

  
  
• 4.
  

  prescription of pharmaceutical agents

The prognosis for recovery from chronic CL-induced redness after removal of lenses and cessation of wear is good. found that, following approximately 5 years of extended hydrogel lens wear, general conjunctival redness resolved within 2 days. In general, removal of any noxious stimulus, including a CL, will lead to a very rapid recovery of eye redness to normal levels.

Papillary Conjunctivitis

This condition refers to the appearance of localized swellings, or papillae, on the tarsal conjunctiva. Papillae are primarily observed in the upper eyelid and can be viewed only by everting the lid. Rarely, papillae can be observed on the lower tarsus by pulling the lower lid firmly down. In soft lens wearers, papillae are more numerous; they are located more towards the upper tarsal plate (i.e. closer to the fold of the everted lid), and the apex of the papillae takes on a more rounded form ( Fig. 38.19 ). In rigid lens wearers, papillae are flatter and are located more towards the lash margin, with few papillae being present on the upper tarsal plate. Papillae often appear as round light reflexes, giving an irregular specular reflection ( ).

Everted eyelid revealing the presence of contact lens-induced papillary conjunctivitis.

(Courtesy C. D. Euwijk, Bausch & Lomb Slide Library.)

In the early stages (less than grade 2) of CL-induced papillary conjunctivitis (CLPC), the tarsal conjunctiva may be indistinguishable from the normal tarsal conjunctiva apart from increased redness. In advanced cases (greater than grade 2), papillae can exceed 1 mm in diameter and often take on a bright-red/orange hue. The distribution of papillae can be more readily appreciated with the aid of fluorescein ( Fig. 38.20 ). The hexagonal/pentagonal shape is lost in favour of a more rounded appearance, with a flattened or even slightly depressed apex or tip. A tuft of convoluted capillary vessels is often observed at the apex of papillae; this vascular tuft will typically stain with fluorescein. Other signs in severe CLPC (greater than grade 3) include conjunctival oedema, excessive mucus and mild ptosis. The cornea may display punctate staining and superior infiltrates. Injection of the superior limbus may also be apparent.

Distribution of papillae as revealed by fluorescein (same eye as in Fig. 38.19 ).

(Courtesy C. D. Euwijk, Bausch & Lomb Slide Library.)

have proposed that two distinct clinical presentations of CLPC are observed in hydrogel lens wearers: local and general. This classification is based on location and extent of papillae, whereby CLPC is classified as local if papillae are present in one to two areas of the tarsal conjunctiva and general if papillae occur in three or more areas. CLPC is less commonly associated with silicone hydrogel lens wear ( ).

There is general concordance between the severity of signs and symptoms. In the early stages of CLPC, patients may complain of discomfort towards the end of the wearing period, slight itching, excess mucus upon awakening, intermittent blurring or a slight but nonvariable vision loss while wearing lenses. As the condition progresses, patients report itching, discomfort and excessive lens movement.

Key factors implicated in the aetiology of CLPC include lens-induced mechanical irritation and immediate and delayed hypersensitivity. There is often a link with MGD, and atopic patients may be more susceptible to developing the condition.

Treatment options include:

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  altering the lens material

  
  
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  replacing lenses more frequently ( )

  
  
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  altering or eliminating the care system

  
  
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  improving ocular hygiene

  
  
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  treating any associated MGD

  
  
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  prescribing pharmaceutical agents such as soft steroids (e.g. loteprednol etabonate), mast cell stabilizers (e.g. 4% cromolyn sodium), combined antihistamine/mast cell stabilizers (e.g. olopatadine hydrochloride 0.1% or ketotifen fumarate 0.025%)

  
  
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  dispensing ocular lubricants for symptomatic relief

  
  
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  reducing wearing time

  
  
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  suspending or ceasing lens wear

Compared with planned-replacement hydrogel lenses, daily disposable hydrogel lenses reduce the risk of papillary conjunctivitis by 50% ( ).

The prognosis for recovery from CLPC after removal of lenses and cessation of wear is good, with symptoms disappearing within 5 days to 2 weeks of lens removal and redness and excess mucus resolving over a similar time course. Resolution of papillae takes place over a much longer time course – typically many weeks and as long as 6 months. The more severe the condition, the longer is the recovery period. In the longer term, however, the prognosis is less good. The condition can recur, especially in atopic patients who appear to have a propensity for developing CLPC.

Limbal Redness

Assuming that a given case of eye redness is lens related, it is necessary to determine whether the source of the problem is the cornea or conjunctiva. Conjunctival redness associated with a quiet limbus and absence of pain indicates a primary conjunctival problem. Conjunctival redness associated with an injected limbus and corneal pain indicates more corneal involvement, or indeed a problem that is related exclusively to the cornea. Careful slit-lamp examination of the anterior ocular structures, and inspection of the CL at high magnification, will generally reveal the cause of the problem. It may also be necessary to prescribe different care systems and differentially diagnose the effects of various solutions over time.

In the absence of any clinically observable ocular pathology, corneal hypoxia is the likely cause of excessive limbal redness ( Fig. 38.21 ). Hypoxia stimulates the release of inflammatory mediators from the limbal vessel walls leading to vasodilatation; this is an automatic reaction designed to facilitate a greater flow of oxygenated blood to the distressed tissue. This mechanism fails in the case of the limbus because limbal blood flow contributes little to corneal oxygenation; the cornea derives virtually all of its oxygen supply from the atmosphere. The result therefore is CL-induced hypoxia maintaining chronic limbal vessel engorgement in a vain attempt to reoxygenate the cornea.

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