Contact Lens & Anterior Eye
Volume 35, Issue 1 , Pages 2-8, February 2012

Corneal erosions in contact lens wear

  • Maria Markoulli

      Affiliations

    • Brien Holden Vision Institute, Sydney, Australia
    • School of Optometry & Vision Science, University of New South Wales, Sydney, Australia
    • Corresponding Author InformationCorresponding author at: Brien Holden Vision Institute, The University of New South Wales, Sydney NSW 2052, Australia. Tel.: +61 2 9385 7516; fax: +61 2 9385 7401.
    • ,
  • Eric Papas

      Affiliations

    • Brien Holden Vision Institute, Sydney, Australia
    • School of Optometry & Vision Science, University of New South Wales, Sydney, Australia
    • Vision Cooperative Research Centre, Sydney, Australia
    • ,
  • Nerida Cole

      Affiliations

    • Brien Holden Vision Institute, Sydney, Australia
    • School of Optometry & Vision Science, University of New South Wales, Sydney, Australia
    • Vision Cooperative Research Centre, Sydney, Australia
    • ,
  • Brien Holden

      Affiliations

    • Brien Holden Vision Institute, Sydney, Australia
    • School of Optometry & Vision Science, University of New South Wales, Sydney, Australia
    • Vision Cooperative Research Centre, Sydney, Australia

published online 04 August 2011.

Article Outline

Abstract 

Contact lens wear continues to be the highest single risk factor for microbial keratitis, particularly when worn in the extended wear modality. For microbial keratitis to occur, the presence of at least a bacterial load as well as a break in the corneal surface is required. One such break occurs in the case of a corneal erosion. These well-circumscribed areas of full thickness epithelial loss can occur both with and without contact lens wear, however the risk of infection is greater in the presence of a lens due to its capacity to provide a vector for the entry of bacterial pathogens. While erosions in non-contact lens wearers are thought to result from defective epithelial basement membrane anchoring, the underlying causes during contact lens wear are yet unknown. This article sets out to review corneal erosions associated with contact lens wear, their associated risk factors such as extended wear, the mechanisms that may be responsible for their formation and the factors that differentiate them from other contact lens related adverse events. Appropriate diagnosis and understanding of the relevant pathophysiology is important to the effective treatment and an understanding of the aetiological factors responsible for erosions is critical to the development of preventative strategies and effective clinical care.

Keywords: Contact lens, Corneal erosion, Microbial keratitis, Contact lens adverse events, Extended wear

 

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1. Introduction 

Contact lenses (CLs) are worn by an estimated 140 million people worldwide [1] and are an important alternative to spectacles and laser surgery in refractive error correction. Despite the advent of new, high oxygen permeability, silicone hydrogel materials, CLs continue to cause adverse events which range in severity from asymptomatic micro-infiltrates, to the fortunately rare microbial keratitis (MK) [1], [2]. Several of these adverse events can result in significant morbidity to the wearer [3] as well as interruption or discontinuation of lens wear [4].

Corneal erosions are one of the adverse events that occur in contact lens wear [5], [6], [7], [8], [9], with the associated discomfort and disruption to lifestyle having the potential to cause significant patient anxiety. Episodes of erosions are unpredictable and of varying intensity and duration [7], [10]. In non-CL wearers, erosions are thought to result from defective anchoring of the epithelium to the stroma [11], [12], [13]. Understanding the mechanisms that underpin corneal erosion formation in CL wear is fundamental to establishing means by which they might be prevented. Currently these causes are unknown.

Although not yet proven, a hypothetical link has been made between corneal erosions and MK [7]. Because of this, erosions may have significance that extends beyond their own occurrence. It is therefore important to be clear on what erosions are, how to differentiate them from other adverse events and how to treat them when they occur. This article sets out to review the phenomenon of corneal erosions in CL wear, including their differentiation from other CL related adverse events, and considers current knowledge of the mechanisms underlying their formation and treatment.

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2. Corneal erosions 

2.1. Definition and clinical appearance 

A corneal erosion is a full thickness detachment of epithelium in a localised and well-circumscribed region of the cornea [14], [15], [16] that can occur either with [6], [8], [17], [18], [19] or without CL wear [14], [15], [16]. The reference to “full thickness” in the definition of an erosion relies on inferences drawn from its appearance [6] and the abnormal epithelial basement membrane histology typical of non-CL related recurrent erosions [11], [20]. To date however, there have been no studies confirming that this is a consistent clinical feature of erosions in CL wear [16]. Clinically, an erosion is usually observed as an absolute defect that stains with sodium fluorescein (Fig. 1) with no underlying infiltrates. Alternatively, an area where the epithelium is detached, but still remains adherent at its borders may be seen (Fig. 2). Presumably, this represents an earlier stage in development and is analogous to a blister of the skin where the raised epidermis at the centre of the lesion eventually sloughs off to expose the underlying dermis (Fig. 3).

2.2. Size and location 

The size of lesions may range from 0.1mm in diameter, to macro-erosions that cover large areas of the cornea [14] (Fig. 1, Fig. 2). Observing with fluorescein and a Wratten filter reveals immediate stromal glow, suggesting that the full thickness of the epithelial barrier has been breached. In cases where the epithelium is still loosely adherent, the lesion will appear elevated (Fig. 2). When the defect is absolute (Fig. 1), fluorescein will both pool in, as well as stain, the floor of the hollow area, which most likely represents the basement membrane.

Erosions may occur in all areas of the cornea and multiple lesions can present at the same time. It has been found that 87.5% localize inferiorly [15] with the most common location being close to the midline, just below the pupil [16]. This is also the region where basement membrane changes are also found to occur most commonly [21].

2.3. Associated signs and symptoms 

While it is not unusual for erosions to occur in the absence of accompanying symptoms [7], limbal and bulbar hyperemia may be evident in the affected sector and photophobia and tearing [15], [16] are common. Importantly, there is no mucopurulent discharge, a useful differentiating factor with respect to corneal infection [6]. A delayed inflammatory response has been reported in some cases [6].

When contact lenses are present, wearers may experience a foreign body sensation, particularly upon awakening if using CLs for extended wear (EW). Alternatively, there may be a sharp pain upon lens removal, followed by a foreign body sensation that is exacerbated by blinking. Lenses may also be difficult to remove, possibly indicating decreased movement or even binding, especially if worn during sleep.

2.4. Incidence 

CL related corneal erosions have been reported with both hydrogel and silicone hydrogel materials [5], [6], [7], [8], [17], [18]. Rates in daily wear (DW) are very low, with one study reporting 0.04 events per 100 participant-months [5], which equated to only a single case. A second study reported 0.01–0.05% per visit [7], with daily disposables being free of events [7]. Although these two studies report on the incidence using difference measures, both indicate a low rate in DW. In EW, erosions occur much more frequently at 0.6–2.6% of visits overall. Silicone hydrogels have a higher rate (0.95–1.68% of visits) than conventional hydrogels at (0.05–0.35% of visits) [7]. Sixty-eight percent of erosions in this study occurred within the first three months of adaptation to lens wear. The incidence of erosions in orthokeratology is unknown.

2.5. Aetiology of contact lens related erosions 

Adhesion of the corneal epithelium to the stroma is mediated by hemidesmosomes, basal laminae, anchoring fibrils and anchoring plaques. The mechanisms that result in the corneal adhesion complexes (Fig. 4) being overwhelmed by the action of the lens to produce an erosion, are yet to be understood. According to the Collins dictionary, erosion is “the wearing away of rocks or soil by the action of water, ice or wind” [22]. Thus in geology the process is a gradual one. For the cornea however, the sudden appearance of well-circumscribed, full-thickness epithelial loss suggests that any causative external force is acting more abruptly. Possibly there is also a more gradual, accompanying internal process that weakens the corneal adhesions such that they subsequently “give way” under suitable provocation, such as may occur for example, with a bound lens. The following reviews the currently known causes of corneal erosions, with particular focus on the mechanisms hypothesized to be associated with CL wear.

  • View full-size image.
  • Fig. 4. 

    Schematic of the corneal adhesion complexes: anchoring filaments extend through the basement membrane and emerge as anchoring fibrils in the stromal side, forming an intertwining network in the anterior 2μm stroma [65]. These anchoring fibrils insert into anchoring plaques. All these factors are termed the “adhesion complex” [65]. Type VII collagen is the anchoring fibril collagen, its domain being in the lamina densa and in the anchoring plaques [20], [65]. Schematic courtesy of Dr Cathleen Fedtke and adapted from a diagram by Dr Michele Madigan.

2.5.1. The bound lens 

Lens adhesion to the cornea has been hypothesized as a possible aetiology for formation of erosions. The suggestion is that when a lens becomes bound to the cornea, as commonly happens during overnight wear [23], an attachment forms between an area of epithelium and the lens surface. When the eye opens and blinking is resumed, this attachment creates a mechanically induced corneal erosion by pulling a “plug” of epithelium away from its surrounds as lens motion recommences [17]. While no studies are known to have tested this hypothesis, it has been demonstrated that mechanical removal of the epithelium in healthy corneas requires significant effort [20]. Any suitable lens/cell adhesion would thus need to be quite tenacious to be effective and it is unclear how such a bond might develop in vivo. Concurrent destabilization of the epithelial adhesion complexes thus seems to be necessary so that the traction forces created by the lens motion would be sufficient to precipitate an erosion. Possibly the presence of the lens during EW is responsible for this activity [24].

2.5.2. Lens thickness and water content 

Very thin high water lenses have been associated with erosions and corneal staining [8], [25]. In work done in the 1980s, one solution to avoiding overnight oedema was to use very thin (22–60μm) high water content hydrogel lenses [8], [26]. However, these 75% water content lenses caused lesions in the central or in the central inferior cornea which were described as erosions [8], [26]. As their location coincided with the thinnest part of the lens and where the tear film was deemed to be thinnest and least stable, the mechanism proposed was that lens dehydration exacerbated thinning of the post-lens tear film resulting in mechanical damage to the epithelial surface. The fact that lesions were less severe in situations of high humidity lent support to this theory [8], [25].

2.5.3. Biochemistry of the cornea 

An upregulation of the collagen degrading enzymes known as matrix metalloproteinases (MMPs) has been associated with corneal erosions in non-CL wearers [27], [28]. This family of enzymes function to maintain and remodel the tissue architecture [28], [29] and are so called because of their ability to degrade the structural proteins of the extracellular matrix [30]. The MMPs have been implicated in diverse physiological processes including embryonic development, tissue morphogenesis and wound repair, as well as pathological systems including inflammatory diseases [31], the autoimmune blistering condition epidermolysis bullosa [30], rheumatoid arthritis [30], [31] and the progression of cancer due to the breakdown of structural barriers [30].

In the cornea, the controlled presence of MMPs is important in maintaining homeostasis. Their uncontrolled production can have collagen degrading effects however [28], and theoretically, this might contribute to erosion formation [27]. MMP-9 is the primary matrix-degrading enzyme produced by basal corneal epithelial cells and neutrophils [32] and is known to be active against major components of the epithelial basement membrane such as collagen type VII [33]. As the fibrils responsible for anchoring the basement membrane to the stroma are composed of Type VII collagen, this activity may result in a weakening of these attachments, contributing to the cascade of events that cause corneal erosions [27], [34]. It is of note that upregulated levels of MMP-9 have been associated with other epithelial defects such as those seen in corneal ulceration [32], [35], ocular rosacea [36], thermal injuries [37] and pterygia [38].

MMP-9 can be inhibited, and hence regulated, by binding to molecules such as Tissue Inhibitors of Metalloproteinase-1 (TIMP-1) or nonspecific inhibitors such as α-2-macroglobulin [39]. The ratio of MMP to TIMP is an important indicator of how well the potential for matrix degradation is regulated at any particular time and delayed wound healing or collagen degrading effects may ensue when the balance becomes disturbed [40]. Some treatment strategies for corneal erosions are thus directed at inhibiting MMP-9 so as to prevent the degradation of the basement membrane components [36], [41].

It has been shown that there is a substantial upregulation of MMP-9 prior to awakening [42], [43], compared to the levels found in the open eye and this is further evidence that the ocular surface is most at risk of developing corneal erosions during sleep [16]. How CL wear affects this diurnal variation has yet to be established.

2.5.4. Bacterial load 

The observation that a protease derived from the bacterium P. Aeruginosa causes epithelial erosions when injected into rabbit corneas [44], [45] has led to the suggestion that an increased bacterial load may be an important factor in the pathology of erosions in human eyes. During wear, CLs isolate the epithelium from the defense mechanisms of blinking, tear flow and the antimicrobial agents in tears [46], [47]. This reduced flow and exchange of tears under the lens may contribute to an increased concentration of microorganisms and their toxins, hence augmenting their impact on the ocular surface [48]. Pseudomonas aeruginosa is the most common cause of keratitis during CL wear [3], [49], [50] and has many factors which help it initiate and maintain infection [49]. One feature is an ability to produce proteases capable of degrading the epithelial adhesion complexes [45]. Okamoto et al. showed that bacterial proteinases, such as P. aeruginosa elastase, V. cholerae proteinase, and thermolysin, activate proMMPs and hence contribute to matrix degradation [51] and Tang et al. demonstrated that Pseudomonas aeruginosa small protein (PASP) causes erosion like defects by cleaving corneal collagen [45]. Bacterial proteinases thus appear able to contribute to, or even initiate tissue damage and this interference with the integrity of the connective tissue exacerbates the inflammatory process. The formation of erosions seems to be one manifestation of this activity.

2.5.5. Reduced epithelial density 

As mentioned above, Madigan and Holden have shown that, the epithelium of hydrogel CL wearing eyes is easier to remove than non-CL wearing eyes [24]. This effect was associated with a reduction in the number of hemidesmosomes, which in turn was due to reduced epithelial density under the long-term hypoxic conditions prevailing during the study. Hypothetically, conditions such as these could contribute to erosion formation by increasing the chances of epithelial cleavage anterior to the basement membrane [20].

2.6. Association with infection 

MK is a rare occurrence in healthy eyes, with CL wear posing the highest relative risk [52]. The incidence of MK has been estimated as 11.9 per 10,000 in daily wear (DW) silicone hydrogels as opposed to 25.4 per 10,000 in EW. This excess risk continues to be a major limiting factor for the EW and continuous wear modalities [53].

While a direct link between CL induced erosions and progression towards MK has not been proven, only one case ever having been reported where multiple central corneal “lesions” coalesced into a central ulcer [9], there is circumstantial evidence suggesting that such may be the case. Calculation of the theoretical rates at which corneal erosions occur concurrently with lenses that are contaminated with gram-negative bacteria, shows that this is higher with EW, at 24.8–60.0 per 10,000 people, than in DW at 1.6–16.4 per 10,000 [7]. Interestingly, these rates are comparable with the frequency of MK in both situations [2], the implication being that both a corneal erosion and bacterial contamination need to be present for infection to occur. Worthy of note in this analysis is that none of the contact lens induced erosions in the series reported by Willcox et al., was associated with a gram-negative lens contamination [7].

The risk associated with the presence of a corneal erosion, particularly in CL wear, is that the natural barrier of the cornea to infection is no longer intact, hence allowing the potential for entry of pathogens and inflammatory cells. The avid binding of Pseudomonas to injured or traumatized areas of the corneal epithelium has been previously established [50] and CLs may heighten this propensity by inducing surface cell desquamation and exposing deeper corneal layers. Preventative pharmaceutical management in the presence of an epithelial erosion would therefore seem prudent to prevent consequences such as infection or uveitis [54], although it is clear that other protective mechanisms, such as antimicrobial factors in the tears, are also present [55].

2.7. Prognosis and recurrence 

CL-induced corneal erosions usually heal within several hours (Fig. 5) to 1–2 days of lens discontinuation [6] and do so with no scarring. Careful observation of the patient with a corneal erosion is necessary to ensure that inflammation or infection does not result [6].

  • View full-size image.
  • Fig. 5. 

    Time lapse of a contact lens wearer presenting with corneal erosion. The patient presented complaining of difficulty removing her contact lens. A: Central corneal erosion immediately after lens removal; B: Appearance after 3h; C: appearance of erosion after 7h suggests a healed erosion with disturbed epithelial staining overlying this.

Epithelial abrasion is followed by an initial sheet-like movement of individual epithelial cells and a subsequent landslide-like movement of the remaining epithelium [29]. After wounding, new anchoring fibrils and hemidesmosomes provide secure attachment of the epithelium to the basement membrane [40]. As complete adherence to the underlying basement membrane may not occur for a few days, temporary discontinuation of CL wear is advised until the area surrounding the erosion settles and secure adhesion is regained.

The rate of recurrence of corneal erosions related to CL wear is unknown. In non-CL wearers, where erosions are recurrent, the median frequency of the attacks is every 60 days [14] with 24% occurring weekly, while 51% occur monthly [14]. The recurrence of corneal erosions following trauma has been estimated as 1:150 [14].

2.8. Preventative strategies 

Preventative strategies include potentially screening CL wearers with in vivo confocal microscopy for co-existing subclinical epithelial basement membrane dystrophies prior to lens wear in order to identify those likely to progress to erosion in the presence of a lens. Moreover, the increased risk of erosions in EW, particularly during the adaptation period, suggests that greater vigilance is required both by the eyecare practitioner and the CL wearer when lenses are worn in the extended modality.

2.9. Treatment 

Management of corneal erosions has three main aims: to reduce the pain in the acute phase, prevent infection and promote re-epithelialisation and re-establishment of the basement membrane [56]. Currently however, there does not appear to be a consensus on the best method of treatment [57].

2.9.1. Lubricants 

Most patients respond to topical formulations such as lubricating drops, gels and ointments to prevent the re-occurrence of erosions [6], [57]. These agents work by keeping the eye lubricated during rapid eye movement and on opening in the morning, particularly in those prone to lens adhesion [6]. In cases of active erosions, they may also minimize the interaction of the eyelid with the eroded corneal surface.

2.9.2. Therapeutic drugs 

Once an erosion has been diagnosed, prophylactic topical antibiotics, as well as careful monitoring are advisable to ensure that inflammation or infection do not result [6], [18]. Some clinicians have proposed using hyperosmotic agents to reduce epithelial oedema [54] and corticosteroids and doxycycline have also been utilized to inhibit the activity of MMPs [36], [41].

2.9.3. Bandage CLs 

In CL related cases, discontinuation of wear usually brings resolution within several hours to 1–2 days [6]. Careful monitoring over the first 24h is warranted to check for the development of infection. Paradoxically, non-CL wearers with recurrent corneal erosions are often fitted with a bandage CL [58]. The purpose of bandage lenses is to protect the eroded area from the shear forces of the eyelids during the blink and during random eye movements during sleep [59]. This is also intended to allow for the regenerated epithelium to develop cell-to-cell adhesions without the disturbance of the eyelid [59]. These patients also should be monitored for MK [57]. In a Cochrane review, bandage CLs were found to be inferior to lubricant use [57]. Ozkurt and colleagues followed a group of 37 patients with either bullous keratopathy, recurrent corneal erosions, filamentous keratitis, corneal melting after surgery, lamellar laceration or chemical trauma [60]. All patients were fitted with Night & Day silicone hydrogel lenses (CIBA VISION, Duluth, ATL, USA) as a therapeutic bandage CL. Of these patients, 84% of patients had complete healing. The bandage lens provided pain relief in 91.16% of patients. Complications from the CL wear in the form of corneal infiltrates resulted in 3 patients.

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3. Differential diagnosis 

Appropriate diagnosis of erosions is important to the effective treatment and prevention of sequelae. The following differential diagnoses of corneal erosions are listed in order from most to least serious.

3.1. Microbial keratitis 

An important differential of corneal erosions is MK, which is an ocular emergency. Microbial keratitis is characterised by progressive excavation of the epithelium, Bowman's layer and stroma with infiltration and necrosis of tissue [19]. Clinical signs include mucopurulent discharge, satellite lesions, lid oedema and conjunctival chemosis along with anterior chamber reaction and occasionally a hypopyon. The location will most likely be central and paracentral [52] but can occur anywhere, with a size greater than 1mm in size. Without aggressive treatment, the lesion worsens despite lens removal and the pain will be increasing and quite severe. Patients will present with progressive pain, photophobia, swelling and discharge [52]. In a study by Keay et al., 25% of patients with MK were found to have had previous episodes requiring urgent attention such as ocular trauma and foreign bodies [52]. Rigorous treatment with fortified antibiotics, for example, tobramycin 1.3% and cefazolin 5%, along with cycloplegia and analgesia are indicated. Microbial keratitis resolves with a corneal scar and an irregular cornea with vision loss if the scar is in the visual axis.

3.2. Contact lens peripheral ulcer 

A contact lens peripheral ulcer (CLPU) is a round anterior stromal focal infiltrate with diffuse infiltration [61] and overlying corneal staining and delayed stromal glow. Unlike erosions, CLPUs represent an inflammatory reaction of the cornea characterized by focal excavation of epithelium, infiltration and necrosis of anterior stroma [19]. Bowman's layer remains intact however [61]. Bulbar and limbal redness will be present, along with the symptoms of watering and pain [61] but a CLPU will not have the mucopurulent discharge or the photophobia seen in MK. Lid oedema and chemosis are not usually present, however there may sometimes be an anterior chamber reaction. The location, as the name suggests, will usually be peripheral. CLPU sufferers will experience immediate relief on CL removal and resolution can be within 7 days [19], [62] though the majority take 2–3 weeks [19]. Unlike erosions, cases of CLPU will most often resolve with a bulls eye scar [19], [61]. Topical antibiotics are prescribed occasionally as prophylaxis, while regular saline rinses combined with cold compresses and analgesia are used to alleviate symptoms [19]. It is hypothesised that the initial epithelial break occurs either due to epithelial injury or due to dissolution of the epithelial layers by biochemical factors [61]. The condition may recur with CL wear [19].

3.3. Superior epithelial arcuate lesions 

Superior epithelial arcuate lesions (SEAL) are raised linear or arcuate excavations that occur in the superior cornea, in the region covered by the upper eyelid. Forty eight percent of cases will have coalescent staining, 35% stromal glow and 50% infiltrates [63]. In 39% of cases there will be a foreign body sensation, while 35% will be asymptomatic [63]. Treatment consists of temporary discontinuation of lens wear and ocular lubricants. Prophylactic antibiotics are prescribed in severe cases. Resolution occurs within 1–9 days, taking longer if there are infiltrates present. Although there is generally no scar, 50% recur.

3.4. Punctate epithelial staining and solution induced corneal staining 

There has been some confusion regarding the definition of corneal erosions with the term “punctate epithelial erosion” occasionally being used to describe diffuse, epithelial damage that has a punctate appearance when stained with sodium fluorescein. An example of punctate staining is that seen in solution toxicity to lens care solutions (Fig. 6) [64]. This kind of presentation affects only the uppermost layers of the epithelium and does not merit designation as “erosion” which typically extend to the deeper layers, often expose the basement membrane and result in immediate stromal glow when stained with sodium fluorescein.

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4. Conclusions 

Epithelial erosions are a relatively rare complication of contact lens wear that have potentially serious consequences such as MK. Their aetiology is poorly understood at present, but once diagnosis has been made, treatment strategies are effective in restoring epithelial integrity, preventing infection, and reducing discomfort.

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Conflict of interest 

This work is original, has not been published and is not being considered for publication elsewhere. There are no conflicts of interest for any of the authors that could have influenced the results of this work. The first author is supported by the Australian Government through the Australian Postgraduate Award and the Brien Holden Vision Institute through a postgraduate grant to cover facilities and supervision. She is also supported by the American Optometric Foundation, the George & Jill Mertz Foundation and CIBA VISION through the William C. Ezell Fellowship, the Cornea & Contact Lens Society of Australia through a Postgraduate Award and the OVRF-Maki Shiobara Scholarship. The first author is a member and fellow of the British Contact Lens Association. All authors have contributed significantly to the project and subsequent drafting, revising and approval of the final version submitted.

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PII: S1367-0484(11)00100-7

doi:10.1016/j.clae.2011.07.003

Contact Lens & Anterior Eye
Volume 35, Issue 1 , Pages 2-8, February 2012

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