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Corneal Infiltrative Complications Associated With Contact Lens Wear
By By Joel A. Silbert, O.D., F.A.A.O.

Self-Assessment Examination Print Version

Release Date: April 15, 2004

Expiration Date: April 30, 2005

Goal Statement: Corneal infiltrates associated with contact lens wear may present from a variety of causative factors. A number of distinct sterile keratitis entities with differing clinical presentations will be discussed, including CLPU, CLARE, infiltrative keratitis (IK), asymptomatic infiltrative keratitis (AIK), and asymptomatic infiltrates (AI). Careful examination techniques are necessary to make an appropriate differential and tentative diagnosis of these relatively benign conditions, as well as to distinguish them from the rarer but potentially sight-threatening infiltrative ulceration known as microbial keratitis (MK).

Faculty/Editorial Board:  Joel A. Silbert, O.D., F.A.A.O.
Professor of Optometry
Director, Cornea & Specialty Contact Lens Service
The Eye Institute
Pennsylvania College of Optometry
Credit Statement: This course is COPE-qualified for 2 hours of CE credit. COPE ID: 11354-CL.
Please check with your state licensing board to see if this approval counts toward your CE requirement for relicensure.
Joint-Sponsorship Statement:  This continuing education course is joint-sponsored by the University of Alabama.
Disclosure Statement: Dr. Silbert has no relationships to disclose.

This course is supported by an unrestricted educational grant from Ciba Vision.

AS AN AVASCULAR and transparent tissue, the cornea and its overall structural integrity remains the principal criterion by which clinicians judge the safety of contact lens wear. Much has been written of the cornea's need for adequate levels of oxygen when wearing contact lenses (EOP)1 as well as the ability of a wide array of contact lens materials to deliver it (Dk, Dk/t).2 Our current understanding of contact lens-associated hypoxia has led to the development of outstanding high-Dk lens materials, both in gas permeable and silicone hydrogel polymers, that can keep the cornea free of lens-induced hypoxia in daily wear (DW) as well as in continuous wear (CW).


In 1980, Mertz3 described the physiological swelling response of the cornea during eye-closure in sleep to be about 4%. In 1984, Holden and Mertz4 were the first to estimate the minimum oxygen transmissibility (Dk/t) requirements for a contact lens worn overnight to limit corneal edema to this 4% physiologic level, to be 87 barrers. [Note: A barrer is the unit of oxygen transmission. 1 barrer = 1 x 10­9 (cm x ml O2) / s x ml x mmHg.] In 1988, La Hood et al5 refined the baseline physiologic sleep level of corneal edema to 3.2%. This result, later confirmed independently by Harvitt and Bonanno6 in 1999, led to our most current understanding that minimum oxygen requirements for safe extended wear are 125 barrers. The FDA approval in 2001 of two new silicone hydrogel lenses for use as 30-day continuous wear lenses is a testament to many years of research leading to a new class of materials. These were CIBA Vision's Focus Night & Day (lotrafilcon A), with a Dk/t of 175 barrers, and Bausch & Lomb's PureVision (balafilcon A), with a Dk/t of 110. These silicone hydrogels, with Dk/t levels of four to six times those of traditional hydrogel lenses, have significantly reduced overnight corneal swelling compared to conventional extended-wear hydrogel lenses, and have demonstrated overnight corneal edema levels comparable to near physiologic levels (with no lens wear overnight).

Hypoxic EW Complications

By essentially eliminating hypoxia during sleep, silicone hydrogels have also eliminated some traditional complications of extended wear. These include: stromal striae and folds,7 limbal hyperemia,8 limbal vascularization,9 myopic creep,10 and epithelial microcysts.7,11,12 Epithelial microcysts, the tiny inclusions observed in the deep epithelial layers of the paracentral to mid-peripheral cornea, are a direct result of EW-induced hypoxia. It should be noted that when patients with chronic hypoxia are refitted from low-Dk EW to high-Dk CW silicone hydrogel materials, there is likely to be a short-term increase in numbers of microcysts, due to the increased metabolic activity from increased oxygenation of the cornea. This apparently paradoxical "rebound effect" may be seen during the first few weeks after refitting, but will gradually reduce over a two- to three-month period, to the point of complete elimination.12 (It should also be mentioned that because microcysts are very small, they could be mistaken for corneal infiltrates. Clinicians must carefully inspect the cornea using biomicroscopy to differentiate the epithelial and vesicular nature of microcysts as opposed to the more opaque, non-vesicular appearance of infiltrates that more often occur in the subepithelial and anterior stromal layers.)

Infiltrative Complications

Perhaps the most vexing complications of contact lens wear involve the appearance of corneal infiltrates. The reason for this, of course, is illustrated by the following: Infiltrates may present benignly as a few clusters of inflammatory cells in the cornea of an asymptomatic lens-wearing or non-lens-wearing patient, representing a non-infectious subclinical response to environmental antigens. On the other hand, after starting out like the prior description, infiltrates may densely accumulate in the stroma and be associated with corneal staining, mucopurulent discharge and tissue necrosis as a consequence of culture-positive microbial keratitis (MK). The latter condition is of the greatest alarm because of its sight-threatening potential. However, as an adverse event, MK is quite rare, due to the outstanding defense mechanisms of the cornea and adnexae. Early events in the development of MK, however, may appear much the same as inflammatory but non-infectious adverse events, such as CLARE (contact lens acute red eye) or CLPU (contact lens-induced peripheral ulcer). The contact lens practitioner must be able to differentiate these conditions via careful history and assessment, proper examination techniques, and appropriate understanding of the respective adverse infiltrative responses that are most likely to present clinically with a given lens-wearing modality. In addition, the clinician must also be familiar with other aspects of corneal and systemic disease that could also produce an infiltrative response unrelated to contact lens wear.

What Are Corneal Infiltrates?

Corneal infiltrates are single or multiple discrete aggregates of gray or white inflammatory cells that have migrated into the normally transparent corneal tissue. They may migrate from the limbal vasculature or from the tears in response to local tissue damage and secondary chemotactic factors, from antigens and toxins from the environment or from contact lens solutions, or from microbial organisms themselves.13 Infiltrates are typically polymorphonuclear leukocytes (neutrophils) but may also contain lymphocytes and macrophages.14 In contact lens wear, infiltrates are most often sterile (non-infectious), but can also be infectious. Distinguishing sterile infiltrates from an active infection of the cornea is often difficult, and in the absence of a culture is often based on the clinician's assessment of the patient's symptoms, size and location of the lesion, presence or absence of corneal staining, and presence or degree of anterior chamber reaction. Mondino and Weissman et al have often warned that in assessing sterile from infectious contact lens infiltrative lesions, the clinician should not rely upon size or location, as all infections begin as small infiltrates,15 and a large percentage of infectious corneal ulcers may present peripherally.16

Corneal subepithelial infiltrates
Careful assessment of infiltrates with the biomicroscope is essential, as their appearance is often subtle and can vary widely in location. Low magnification overview with diffuse illumination should be followed by higher magnification views using direct and indirect illumination techniques. When observing infiltrates, also check for any accompanying signs such as corneal staining, discharge, bulbar or limbal injection, and anterior chamber reaction. Does the patient report pain or irritation, photophobia, tearing, or change in visual acuity? Is there evidence of blepharitis? Non-contact lens wearing patients with chronic blepharitis frequently demonstrate sterile marginal staphylococcal ulcers or infiltrates associated with toxins released by Gram-positive bacteria.17 Although there are differences, this condition is likely related to a complication of hydrogel lens extended wear, the CLPU associated with Gram-positive bacterial colonization of EW contact lenses (both staphylococcal and streptococcal),18,19 more of which will be discussed below.

Because contact lens-associated corneal infiltrates can have such a wide-ranging presentation, both in appearance as well as clinically, it is best to classify and describe them in context with their clinical manifestations.20,21 This classification system has now become widely used and includes:

CLPU (Contact lens-induced peripheral ulcer)
MK (Microbial keratitis)
CLARE (Contact lens acute red eye)
IK (Infiltrative keratitis)
AIK (Asymptomatic infiltrative keratitis)
AI (Asymptomatic infiltrates)

CLPU (Contact Lens-Induced Peripheral Ulcer)

CLPU (contact lens peripheral ulcer)
(Courtesy: CCLRU/LVPEI Guide to Corneal Infiltrative Conditions)

CLPU is a unilateral response of the cornea occurring as a result of colonization of contact lens surfaces by pathogenic Gram-positive bacteria, primarily Staphylococcus aureus and S. epidermidis. Although seen with daily wear lens use, CLPU is more commonly observed with EW usage. Toxins released by the bacteria give rise to a whitish/gray focal anterior stromal infiltrate in the periphery or mid-periphery of the cornea. The round infiltrate can range in size from 0.1mm to 2.0mm,22 and during the acute presentation will show a full-thickness loss of epithelium. Symptoms may be absent, or may be significant with moderate foreign-body sensation, redness and tearing.

Symptoms rapidly decrease, and the epithelium resurfaces over the lesion, leaving a well-demarcated grayish scar. This scar often assumes a "bulls-eye" appearance and gradually fades after six months. A common clinical observation in contact lens practice is the presence of a newly discovered round scar in the peripheral cornea of an established patient wearing EW hydrogel lenses. This shows that the inflammatory events associated with CLPU are often so mild as to escape patients' attention. Approximately 50% of CLPUs present as scars in the absence of symptoms.9

Patients who experience repeat episodes of CLPU are likely to have high levels of S. aureus and/or S. epidermidis on their lids and lashes. Overnight lens wear is best avoided in these patients.23,24 CLPUs are seen in patients wearing EW hydrogel lenses and CW silicone hydrogels. The elimination of hypoxia does not eliminate the risks of this complication.21

Differential Diagnosis

The differential diagnosis for CLPU includes: early MK, marginal keratitis, and corneal phlyctenulosis. Because MK is sight threatening, it is imperative to distinguish it from the benign CLPU. The features of MK that clinically differ from CLPU include:

  • Increasing severity of signs and symptoms after lens wear is discontinued.
  • Irregular infiltrate with raised edges; satellite lesions are common.
  • Mucopurulent discharge, adherent to the lesion.
  • Lid edema.
  • Severe diffuse bulbar and limbal hyperemia.
  • Endothelial reaction.
  • Marked anterior chamber reaction (flare and cells, possible hypopyon)

Unlike MK, CLPUs have milder symptoms and quickly resolve with lens discontinuation, in the absence of therapeutic intervention. However, even though CLPU is non-infectious, the similarity between an active CLPU and an early peripheral MK dictates conservative management for CLPUs. This involves not only discontinuing lens wear, but also prescribing a broad-spectrum topical fluoroquinolone antibiotic (preferably fourth generation, which has good Gram-positive coverage), and extremely close monitoring over the first 24-hour period. (Be sure to schedule an appointment for a one-day follow-up and arrange for a telephone call several hours after seeing the patient to ensure that symptoms are not worsening.)24

CLPUs differ from peripheral corneal hypersensitivity-induced conditions, such as marginal ulcers, and phlyctenulosis, even though they all involve staphylococcal antigen hypersensitivity. Marginal ulcers are typically oval in shape, are located at the 2, 4, 8 and 10 o'clock positions and run parallel to the limbus. Although the infiltrate is always separated by a clear interval, it can be spanned by blood vessels. In distinction, CLPUs can occur at any position in the peripheral cornea.22 There is no clear interval, as infiltrates are seen to stream from the limbal vasculature to the focal infiltrate, and there are no bridging vessels. CLPUs differ from corneal phlyctenules, as there is no raised nodular infiltrate or vascularization.21

MK (Microbial Keratitis)

Microbial keratitis (MK)
(Note the diffuse injection, hypopyon, and adherent mucopurulent discharge.)

MK is a very serious complication of contact lens wear. It can occur with any type of lens wear, with the highest incidence in hydrogel extended wear, and lowest incidence with GP lenses and with silicone hydrogels. The low general incidence of this insidious adverse event is attributable to the excellent ocular defense mechanisms that include: tear flushing, mucus entrapment of microbes, presence of lysozyme and lactoferrin in the tears, the complement protein activation system within the immune complex that aids in microbial capture and opsonization (coating), secretory IgA which prevents microbial adhesion to the corneal epithelium, as well as the physical barrier of the corneal epithelium itself.25 Thus, when MK occurs in a contact lens wearer, a major breakdown in some or all of the cornea's defense mechanisms has taken place, allowing the invasion of pathogens.

Despite the generally low incidence of MK, studies have clearly shown significantly higher rates of MK for patients wearing low-Dk hydrogels on an EW basis and that the risk is worsened as the number of consecutive nights of overnight wear increases.26-30 For this reason, practitioners have for some time discouraged their patients from sleeping in low-Dk lens materials. A large body of ev idence has demonstrated adverse effects of corneal hypoxia on nearly all layers of the cornea. Studies showing reduced epithelial intercellular adhesion as well as the increased levels of adherence of Pseudomonas aeruginosa to exfoliated corneal surface cells in low-Dk soft lenses31 have all contributed to our understanding of the mechanisms leading to MK in contact lens wear.

Studies of high-Dk silicone hydrogels worn on a CW basis have shown reduced levels of Pseudomonas adher-ence,31,32 and it is becoming clear that lenses that eliminate hypoxia and reduce bacterial adhesion will result in a healthier epithelium. While silicone hydrogels will not eliminate the possibility of MK, they are likely to greatly reduce its incidence, perhaps to levels approximating the very low levels seen with daily wear hydrogels.33

Although numerous microorganisms have been associated with MK, it is the Gram-negative Pseudomonas spp., especially P. aeruginosa, that has been implicated in the majority of extended-wear infections involving hydrogels and silicone hydrogels.

Three factors are necessary for MK:

  • Exposure to infectious pathogens.
  • Binding of pathogens to the cornea.
  • In most cases, the presence of a break in the corneal epithelium, facilitating invasion and replication of organisms.

Stromal necrosis occurs in Pseudomonas infections from the liberation of exotoxins, endotoxins, and numerous proteolytic enzymes. The stromal infiltrates with Pseudomonal MK are dense, and accompanied by severe edema, large central epithelial excavation, and mucopurulent discharge clinging to the lesion. There may also be a ring infiltrate from the release of endotoxin.13

Patients presenting with signs and symptoms consistent with MK require immediate medical management. Small (<2mm) ulcers in the anterior stroma usually respond well to topical fluoroquinolone monotherapy, prescribed aggressively according to established protocols. Larger (>2mm) and more severely presenting ulcers, and those that are on the visual axis are better treated with topical fluoroquinolones in combination with fortified antibiotics. Cycloplegics are used to temper the anterior chamber reaction, as well as to prevent posterior synechiae.

Although cultures are often not taken with small peripheral ulcers, they should be obtained whenever lesions are larger than 2mm, are more than one-third the thickness of the cornea, are in the visual axis, and are observed in "at-risk" populations (i.e., the elderly, the immuno-compromised, or monocular patients).33 Cultures should also be taken of the patient's contact lenses and solutions, if available, to increase the chance of obtaining positive identification of the pathogen. Severe cases require referral to an experienced corneal specialist. Early and aggressive treatment of MK can lead to good visual outcomes, although a permanent scar will always be present. Delay in the diagnosis and treatment of MK can lead to severe consequences, including corneal perforation and the need for penetrating keratoplasty. Non-bacterial sources of MK, such as protozoan (Acanthamoeba) and fungal etiologies, may result in much worse outcomes.

CLARE (Contact Lens Acute Red Eye)

A non-ulcerative sterile keratitis associated with colonization of Gram-negative bacteria on contact lenses is known as CLARE. As with MK, it is primarily the Pseudomonas spp. that colonize and adhere to extended-wear lenses, releasing endotoxins and recruiting inflammatory cells.34,35 While contact lenses are commonly colonized by bacteria, this event is not always associated with the presence of infiltrates, indicating that infiltrate formation is probably related not only to the species but also the strain of bacteria, as well as its virulence.36 For example, some strains of P. aeruginosa may be associated with CLARE, and others with MK. In addition, the integrity of the host, i.e. corneal epithelium, may also be a factor that weighs on whether or not an infiltrative response will occur.

CLARE (Contact Lens Acute Red Eye) (Courtesy CCLRU)

Contact lenses themselves, either through mechanical factors or from lens deposits, can also cause injury to the cornea. This can occur in microtrauma by inducing inflammatory cytokines directly, or in the case of deposits, serving as antigens to trigger an immune response leading to infiltrates.37

Although Pseudomonas spp. are most commonly associated with CLARE, other Gram-negative bacteria have also been implicated, including Serratia marscesens and Haemophilus influenzae. As a higher incidence of CLARE occurs in patients with upper respiratory infections involving H. influenzae,38 patients with these symptoms who sleep in contact lenses should be educated to remove their lenses or switch to daily wear.24

The typical scenario for a patient experiencing a CLARE response is that of extended-wear hydrogel use, in which the sleeping patient awakens with uniocular pain (foreign-body sensation), photophobia, tearing and a red eye. Visual acuity is unaffected. Examination reveals sub-epithelial infiltrates in the mid-periphery of the cornea near the limbus, distributed either focally or diffusely. There is no clear interval between the diffuse infiltration and the limbus, with infiltrates appearing to stream from the limbal vessels.21 There is also pronounced limbal injection circumferentially, but no anterior chamber reaction or lid edema. In many cases of CLARE, lenses with insufficient movement are observed. Although CLARE most commonly affects EW wearers of hydrogel lenses, it can occur with well-fitted or immobile lenses of any material or oxygen transmission.21,40,41 Clinicians should also be alert to the observation that inflammatory events such as CLARE and CLPU may be recurrent in some patients. Sweeney et al23 looked at inflammatory adverse events occurring in 116 patients over a three-year period with 30-day continuous-wear silicone hydrogels, and found a recurrence rate of 10% for CLPU and 29% for CLARE.

As CLARE is non-ulcerative and non-infectious, it will subside with removal of contact lenses. Temporary discontinuation, along with ocular lubrication should facilitate reduction of signs and symptoms. However, given the presence of large quantities of Gram-negative organisms, conservative treatment may also utilize prophylactic topical fluoroquinolone antibiosis for the first 24- to 48-hour period, during which time the patient should be monitored.42 Re-assessment of lens fit is warranted in cases where tight-fitting lenses are observed, as well as a switch to daily wear in recurrent cases. 

IK (Infiltrative Keratitis)

Infiltrative Keratitis (IK)
(Courtesy, CCLRU/LVPEI)

The term IK, or infiltrative keratitis, applies to conditions other than CLPU, MK and CLARE, in which there is sudden onset of infiltrative events. Unlike CLARE, which occurs during sleep, IK symptoms occur later in the day. The inflammatory events of IK may develop from a variety of causative factors, including mechanical trauma, Gram-positive bacterial exotoxins, and even from a minor foreign body trapped under the lens.25 Symptoms may vary widely, from severe to non-existent. When no symptoms are present, the term AIK, or asymptomatic infiltrative keratitis, is utilized. When there are signs and symptoms, they may include: tearing, photophobia, foreign-body sensation, injection of the bulbar conjunctiva and limbus, and mild diffuse or small focal infiltrates. Infiltrates are often near the limbus, but can be present anywhere in the cornea. There also may be mild corneal punctate staining.21, 24

Management of IK requires temporary lens wear discontinuation. Lens wear should not be resumed until all signs and symptoms are completely resolved. Medication is usually unnecessary in most cases of IK, with palliative use of preservative-free ocular lubricants. In cases where symptoms are severe, or where there is significant infiltration, the prophylactic use of antibiotics to prevent secondary infection44 or antibiotic/steroid combination drops to mitigate the inflammatory response is sometimes beneficial.24 Because many cases of recurrent IK are secondary to exotoxins released by lid margin bacteria (Staphyloccus spp. and Streptococcus spp.), it is wise to recommend lid hygiene in these cases, and to limit lens wear to daily wear.

AIK (Asymptomatic Infiltrative Keratitis)

In cases of asymptomatic infiltrative keratitis observed in DW, EW, and even among non-lens wearers, the eye is often quiet in appearance. There may be a few small focal infiltrates and/or mild diffuse infiltration in the anterior stroma. There is often accompanying punctate staining, and mild bulbar conjunctival or limbal redness may be observed. AIK may be unilateral or bilateral. In lens wearers, temporary discontinuation will lead to rapid resolution within a week in most cases, and no medication is required.21 

AI (Asymptomatic Infiltrates)

AIK (asymptomatic infiltrative keratitis) (Courtesy, CCLRU/LVPEI)

AI is the most benign infiltrative presentation, with a few tiny focal infiltrates observed anywhere in the cornea, but most commonly in the periphery. The epithelium is intact, and resolution occurs quickly and without complication or need for medication. AI is observed both in contact lens wearers and in non-wearers, and does not appear to have any risk factors or pathogenic cause. It is believed to be due to environmental antigens. Management does not require discontinuation of the lens in most cases, unless multiple infiltrates are observed.21

Lens Care and Non-Compliance

Corneal infiltrates have historically been associated with first-generation soft contact lens care systems, most notably with hypersensitivity and toxicity responses to thimerosal and chlorhexidine.45,46 With the advent of hydrogen peroxide, daily disposable contact lenses, and second- and third-generation chemical care systems, incidence rates of corneal infiltrates have dropped markedly. However, when observed, infiltrates are still significantly associated with inadequate compliance, with sterile infiltrates commonly seen among patients who demonstrate poor contact lens hygiene and among those with case contamination.

Infiltrates have continued to be observed with disposable lenses, not only due to non-compliance with replacement at recommended intervals,47 but also due to the fact that disposable hydrogels neither reduce chronic hypoxia associated with EW, nor are immune to bacterial colonization. This was perhaps best borne out by the finding that there was a significantly higher incidence of corneal infiltrates in wearers of disposable lenses worn on a daily wear basis than among wearers of disposable extended-wear hydrogel lenses.49


Corneal infiltrates associated with contact lens wear may present from a variety of causative factors. These include the mechanical nature of lens wear itself, wearing lenses during sleep, bacterial colonization of lenses, fitting characteristics, replacement schedules, and lens care products. In addition, infiltrative complications may be exacerbated by pre-existing systemic conditions, from pathogens present on the lids and adnexae, and even from the environment.

A number of distinct sterile keratitis entities with differing clinical presentations have been discussed, including CLPU, CLARE, infiltrative keratitis (IK), asymptomatic infiltrative keratitis (AIK), and asymptomatic infiltrates (AI). Careful examination techniques are necessary to make an appropriate differential and tentative diagnosis of these relatively benign conditions, as well as to distinguish them from the rarer but potentially sight-threatening infiltrative ulceration known as microbial keratitis (MK).

The development of high-Dk silicone hydrogels has appropriately invigorated the concept and the reality of much safer continuous wear by the elimination of hypoxia-induced neovascularization, striae, microcysts and limbal hyperemia. However, the clinician must remember that the elimination of hypoxia does not eliminate the mechanical effects of lens wear, nor does it eliminate the potential for infiltrative and inflammatory complications. While these are not sight threatening like MK, they can be the source of significant discomfort and inconvenience. As such, they must be diagnosed accurately and treated both efficiently and aggressively.


   — References —

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