Chapter 27
Complications of Contact Lenses
Erich B. Groos, Jr.
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Contact lenses are visual prostheses worn for the purpose of correcting refractive error. Most contact lenses are worn for cosmetic and functional reasons by those who prefer them to spectacle correction. Patients approach the wear and care of contact lenses with varying degrees of discipline. Complications suffered by contact lens wearers can commonly be attributed to poor lens hygiene or overwear, poor lens fit, or underlying ocular pathology. Management of the latter two risk factors is to some extent under the control of the physician who fits lenses, but day to day management remains the responsibility of the patient. Educating and monitoring each patient for appropriate lens wear and care requires substantial time and effort and; unfortunately, directions for appropriate lens management are frequently ignored.1–5 Patients with higher levels of ametropia tend to be more dependent on contact lens correction and are thus more likely to push the limits of safe contact lens wear.5 More often than not, experienced contact lens wearers become less fastidious over time and gradually abandon basic principles of lens cleaning and disinfection.1

As contact lens use has become more prevalent in the ametropic population, the prevalence of complications as a proportion of emergency eye care visits has increased; yet the overall prevalence of contact lens-related visits remains below 5%.6–8 An eye care specialist who encounters a contact lens wearer with contact lens intolerance must recognize the signs of contact lens-related ocular disease and identify the appropriate cause. Bruce and Brennan9 present a thorough and thoughtful analysis of corneal pathophysiology as it relates to contact lens wear. They separate the forces that cause corneal disease in contact lens wear into four major categories:

  1. Hypoxia and hypercapnia
  2. Allergy and toxicity
  3. Mechanical effects
  4. Osmotic effects

Of these four, the first two account for the majority of complications encountered in practice.

 This chapter contains a review of the complications of contact lens wear in the order in which one might encounter them in the course of an organized examination of a patient. Defective contact lenses may affect vision unrelated to any complication. The eyelids are rarely the site of complications and may show meibomian gland dysfunction, blepharoptosis, or upper eyelid masses. The conjunctival surface is the frequent victim of contact lenses and the solutions necessary for their care. Inflammation secondary to toxicity or allergy occurs in the form of follicular conjunctivitis, giant papillary conjunctivitis, superior limbic keratoconjunctivitis, and other rarer conditions. Chronic inflammation may cause concretions or dry eye. The cornea, upon which the contact lens floats, is the ocular structure most commonly affected adversely by contact lenses. Epithelial alterations include physical damage, vascularization, edema, cysts, and hypoesthesia. Corneal stroma may show edema, infiltrates, vascularization, opacities, infectious keratitis, or ectasia. Endothelial cells may be affected by long-term contact lens wear by forming blebs or exhibiting polymegathism. Finally, there are a few rare intraocular complications associated with contact lens wear that may not owe their cause to lens wear alone.

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Because it is avascular, the cornea relies on gas exchange at the tear-air interface for successful aerobic metabolism. The threshold among individual eyes to suffer hypoxic complications varies widely.10,11 Eye closure and contact lens wear decrease the exchange of oxygen and carbon dioxide at the corneal surface. Oxygen transmissibility (dK/L), which is lens material permeability (dK) divided by lens thickness (L), is the most important variable when determining relative oxygen delivery to the corneal surface through a contact lens.12,13 The exchange of tears under the contact lens also influences corneal oxygen tension. Small diameter rigid lenses of the same or lower oxygen transmissibility may result in less corneal edema than larger diameter soft lenses because of superior tear exchange.13,14 Hypoxia and hypercapnia are less severe in the deep stroma and endothelium, which may obtain oxygen from and discharge carbon dioxide into the aqueous humor.15,16 It is estimated that a dK of 300 would be required to prevent acidosis from anaerobic metabolism of the corneal epithelium, but only a dK of 18 would be required to do the same for the aqueous.16

In the absence of adequate oxygenation, the corneal epithelial mitotic rate decreases causing decreased thickness, microcysts, and increased fragility.9 The compromise in junctional integrity of the epithelial cells that ensues leads to punctate epithelial keratopathy, epithelial abrasions, and increased risk of microbial keratitis. Stromal lactate accumulation from anaerobic metabolism causes increased stromal thickness and disruption of the regular pattern of collagen lamellae leading to striae, posterior stromal folds, and increased light backscattering. Acidosis also increases corneal oxygen requirements, thereby exacerbating corneal hypoxia.17 Long-term stromal hypoxia and hypercapnia create stromal acidosis, which, in the short term, will elicit endothelial edema and blebs and, over many years, endothelial cell polymegathism. Further effects of hypoxia are corneal hypoesthesia and neovascularization of both the epithelium and stroma. Stromal vascularization may evolve to interstitial keratitis, deep opacities, or rarely intrastromal hemorrhage. In some cases of long-term wear, the cornea becomes accustomed to the new oxygen tension, and stromal edema is replaced by stromal thinning.


A spectrum of ocular disorders that are allergic in etiology predispose to contact lens intolerance in certain individuals. Allergic rhinitis and conjunctivitis are risk factors for poor contact lens tolerance.18 The contact lens wearer faces a variety of potential allergens. Contact lenses also encourage adhesion of debris, which remains in contact with ocular tissues and prolongs the exposure to allergens. Contact lens solutions and, in particular, the preservatives within them, induce allergic responses in susceptible individuals.19 Thimerosal hypersensitivity may cause conjunctivitis, corneal epithelial infiltrates, and superior limbic keratoconjunctivitis.9 Reaction to protein deposits on contact lenses may produce giant papillary conjunctivitis resembling that with exposed sutures.19 The toxicity induced by an immobile contact lens is related to the rapid accumulation of metabolic by-products in the anterior corneal layers, which may result in limbal hyperemia, peripheral corneal infiltrates, and keratitic precipitates.9 Further surface damage may be the result of solution toxicity causing various patterns of punctate epithelial keratopathy.


Mechanical forces inducing complications in contact lens wearers may include injuries sustained by improper placement or removal of a lens or those related to contact lens fitting and wear. Steep fitting rigid lenses may induce corneal distortion or leave a surface imprint. In severe cases the corneal surface becomes warped. Tight fitting soft lenses may induce surface wrinkling. Epithelial damage may occur because of debris trapped below the lens. This complication is particularly important considering the preponderance of female cosmetic contact lens wearers.7


Contact lenses increase tear evaporation and decrease reflex tearing, thereby promoting the development of punctate epithelial keratopathy. Surface desiccation impairs ocular lubrication by the tear film, putting the epithelium at risk for mechanical injuries such as abrasions and erosions.

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Choosing the appropriate contact lens type for a particular patient requires careful consideration of refractive error, corneal shape, preexisting ocular disease, and patient preference. The relative risks for complications of soft and rigid lenses using both extended and daily wear routines are important in the decision process. Rigid lenses are associated with fewer overall complications than soft lenses.6,20 Because rigid lenses have a significant adjustment period, failures within the first 6 months are approximately equal for both rigid and soft lenses.21 Risk for complications is directly proportional to the length of uninterrupted wearing time for any type lens.6,26–28 Extended wear lenses are associated with the highest relative risk for all complications except corneal abrasion, which occurs more frequently in the rigid lens population.6,29 Newer silicone polymers with high dK seem to have reduced, but not eliminated, the complications of extended contact lens wear.21–25 Daily disposable soft lens wear appears to provide the greatest safety.29–33


Rigid contact lenses may break or chip to produce punctate epithelial keratopathy, corneal erosions, or corneal abrasions. A warped lens may cause corneal warpage or keratoconus.34 Lens deposits may accumulate inducing focal inflammation and rarely giant papillary conjunctivitis.35 Despite tearing with relative ease, soft contact lenses wreak much less epithelial damage than nicked or broken rigid lenses.29 Hydrogel lenses attract much more protein deposition making them more antigenically potent. A comprehensive review of soft lens defects is beyond the scope of this chapter but can be found elsewhere.36


Rigid contact lenses of both the gas-permeable and polymethylmethacrylate (PMMA) type are effective lenses for the correction of astigmatic ametropia. These lenses deliver better image clarity than soft hydrogel lenses, but their use is limited by the high early drop out rate secondary to discomfort.21 Rigid lenses accumulate less protein and are thus less prone to induce allergic complications. Rigid lenses as a group are associated with fewer severe complications overall than soft lenses.6,7,20 The difference in the rate of infectious keratitis is even greater.20 Extended wear of rigid contact lenses, though encouraging because of their favorable oxygen transmissibility, has been limited by the significant prevalence of lens adherence to the cornea with overnight wear.37,38 Recent developments in rigid lens materials with high dK's and advanced designs have fueled the resurgence of orthokeratology. The short-term safety of this method for corneal flattening has been established, but the continued risk for corneal warpage, infectious keratitis, lens binding, central island formation, and erosion remains to be defined.


Wearing soft contact lenses on a daily basis is a popular method for correction of refractive errors. These lenses present a small relative risk of nonulcerative complications compared to rigid lenses and a lower risk than extended-wear lenses.6 Compared to disposable daily wear lenses, conventional daily wear lenses have a higher rate of complications, excluding ulcerative keratitis, the rate for which is the same for both groups.39 The prevalence of ulcerative keratitis for daily soft lens wear is lower than that for any type of soft extended wear lens and higher than that for daily wear rigid lenses.20,40 Daily disposable soft lenses afford the lowest complication rate of any lens type.29–33


Continuous-wear soft contact lenses are ideal for patients with high refractive errors who wish to see at all times. These individuals are significantly handicapped without their spectacles, making even contact lens insertion difficult. This wearing regimen has become more popular for the general population of lens wearers because the amount of care required is significantly reduced. The minimal care model is taken to the ultimate level with disposable extended wear lenses.

Despite favorable early reviews, extended wear soft lenses have not become the panacea that was expected because of a higher incidence of ulcerative and nonulcerative complications compared to soft and rigid daily wear lenses.6,20,41 The safety of disposable extended wear lenses is better overall than for conventional extended wear, but the risk for infectious keratitis is the same.40 Sterile infiltrates occur more frequently with the disposable extended wear lenses.40 This higher risk for sterile keratitis may skew the results of some trials comparing rates of infectious keratitis for disposable versus conventional lenses. Because of chronic hypoxia related to extended lens wear, many extended wear lens failures are secondary to progressive superficial vascularization.42 Initial fitting with extended wear lenses that move well and have higher dK/L values helps to decrease the number of potential failures.43 The availability of high dK silicone polymer hydrogels has dramatically reduced but not eliminated the complications associated with extended lens wear.22–25


Contact lens correction of aphakia in both the geriatric and pediatric population may be limited by the difficulties of handling the lenses.44,45 Many elderly patients and parents of children lack the manual dexterity necessary to remove lenses on a daily basis. Extended wear soft lenses for aphakic correction, even with enhanced oxygen permeability, have limited transmissibility because of increased center thickness. Major compli-cations observed include neovascularization, apical ulceration secondary to overwear and infectious keratitis.44–46 Rigid daily wear lenses have a 10-fold reduced risk of infectious keratitis compared to soft extended wear in this population, but their use is curtailed by problems with handling, discomfort, and care.45 Coupled with the hypoxic stress on an already surgically compromised endothelium, these risks for many may make secondary intraocular lens implantation a more reasonable option. Improvements in lens implant design and safety of surgery have dramatically reduced the number of aphakic eyes over the last decade.


Hydrogel contact lenses are useful in the treatment of a variety of ocular surface disorders from dry eye to corneal perforation.47,48 The complications one encounters with these lenses are much the same as those with cosmetic extended wear lenses but occur with greater frequency because of an underlying disease process. One contact lens-related complication that may mimic more severe disease-related problems is the immobile lens syndrome.9 Though this syndrome may occur rarely in cosmetic extended soft lens wearers, it most often complicates therapeutic lens wear. As the name implies, the lens becomes immobile and traps debris against the cornea for an extended period of time. The resulting intense inflammatory reaction causes varying degrees of limbal hyperemia, peripheral corneal infiltration, and intraocular inflammation, including keratic precipitates and rarely hypopyon. This effect may be avoided by fitting lenses that move well and have high dK values. If one uses a lens with a high water content, assessment of lens movement within 24 hours is important because these lenses tend to shrink. It is important to consider therapeutic lens wearers separately when compiling data concerning contact lens complications because they may skew the results.

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Eyelid structures lie in direct apposition with contact lenses and exhibit varying degrees of inflammation, both clinical and subclinical. The meibomian glands are situated less than a millimeter from the tarsal conjunctival surface and can be affected by chronic, low-grade mechanical and chemical irritation. Contact lens wearers show significantly more meibomian gland dysfunction than matched controls.49 Although this study was not masked, it supports some authorities' theory that tear lipid abnormalities are an underrecognized cause of contact lens intolerance, particularly in veteran wearers. Meibomian gland dysfunction in a symptomatic contact lens patient with decreased tear break-up time should be treated with moist heat and, in severe cases, with oral tetracycline derivatives. Short-term use of mild topical corticosteroids is helpful in severe cases. In refractory cases, discontinuation of contact lens wear is necessary to break the cycle perpetuated by inflammation. Careful examination for and treatment of causes of periocular inflammation and changes in contact lens care may be required to prevent further exacerbation of the condition. The rapid accumulation of protein deposits in these patients may require a temporary shift to daily disposable lenses. Although meibomian gland dysfunction related to contact lens wear rarely progresses to visual loss, severe cases left untreated show progressive decrease in surface lubrication, leading to an increased risk of infectious keratitis and scarring.


Long-term wear of rigid contact lenses has been reported to cause blepharoptosis in a wide age range of patients. In a two-pronged study, van den Bosch and Lemij50 describe seventeen patients with rigid contact lens-related ptosis. Two of these patients had unilateral ptosis that occurred on the side of rigid lens wear. One of the two wore a soft lens in the fellow, non-ptotic eye. The second part of the study compares the margin reflex distance (MRD) of a group of long-term rigid lens wearers to that of an age-matched control group. The former group has a smaller MRD and more clinical diagnoses of ptosis than the control group. An earlier study describes the surgical pathology of contact lens-related ptosis as levator aponeurosis disinsertion.51


In rare cases rigid contact lenses that were thought to be lost migrate through the conjunctiva at the superior tarsal border of the upper eyelid to present many years later as an upper eyelid mass.52–57 A ring-shaped protrusion with a hole in the center located on the conjunctival side of a lid mass suggests the diagnosis.52 Histologic examination reveals a cystic cavity lined with epithelium, scar tissue, and chronic inflammation.53–55 The clinical presentation is that of an eyelid tumor or chalazion. In at least one case the contact lens presented spontaneously from the mass.54 Computed tomography scanning will not reveal the lens if present; therefore, one must inquire regarding a previously lost contact lens in these cases.56 The lens may also migrate into the orbit to cause an orbital mass.57 Of all reported cases, 21 lenses were found in the upper lid, 2 migrated into the orbit, and 2 extruded from the lid.57

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Conjunctival injection in a contact lens wearer often seems to be the norm rather than the exception. With all forces both mechanical and chemical conspiring to induce inflammation, it is surprising that the prevalence of severe conjunctival inflammation is not greater. In 1980, before the widespread use of hydrogel or gas-permeable contact lens materials, Korb et al.58 found a significantly higher prevalence of elevated papillae in long-term PMMA wearers than in a large control group. Considering that a soft contact lens behaves like a small sponge, it is not surprising that a soft contact lens wearer is five times more likely than a rigid lens wearer to present with a hypersensitivity or toxicity-related disorder.6 Hypersensitivity and toxicity accounted for 387 out of 1104 (35%) emergency admissions to a tertiary eye hospital with contact lens-related problems.6 Of that number approximately two-thirds were conjunctivitis.


Continuous friction and chemical forces of contact lenses on the conjunctival surface promote the formation of mucus in quantities higher than in those who do not wear lenses. On a microscopic level the number of goblet cells is increased over that of normal controls.59 The number of nongoblet cells lining the epithelium that contain mucous vesicles is increased in contact lens wearers relative to normal controls.59 Only in rare cases does overproduction of mucus result in loss of the ability to wear contact lenses.


As discussed previously, contact lenses have been associated with an increased risk of meibomian gland dysfunction with its attendant decrease in tear surface integrity. In addition to a loss of surface lubrication, the loss of lipid layer integrity allows increased aqueous evaporation; a process further accelerated by contact lenses, particularly those with high water content. The hydration required by these lenses absorbs water from the surrounding tear lake. Hydrogel lenses and, to a greater extent, rigid lenses cause corneal hypoesthesia, which decreases basal and reflex tear secretion.60 The combination of lipid, aqueous, and mucin abnormalities caused by contact lens wear puts the wearer at higher risk for dry eye.61 Treatment should be directed toward symptomatic patients with regard to specific abnormalities identified on careful examination. In most cases, the dry eye is multifactorial and may not respond to artificial tear therapy alone. Contact lens cessation will often allow more rapid resolution of dry eye symptoms. Once discontinued, lenses may then be worn with protective measures prescribed to decrease recurrences.


Chronic contact lens wear in the presence of significant daily exposure to particulate matter promotes the phagocytosis of particles by cells of the conjunctival epithelium, primarily in the inferior fornix. Contact lens wearers in industrial situations, where there is significant dust exposure, and those who wear makeup that spills into the tear lake daily are at risk of developing concretions. In most instances concretions are benign, but the engulfed material may erode through to irritate the ocular surface. Concretions that stain with fluorescein after 5 minutes in a symptomatic patient may be removed under topical anesthesia.


Toxicity of various contact lens-related chemicals to the ocular surface causes bulbar conjunctival injection and papillary conjunctivitis in the fornices, usually more pronounced inferiorly. Also known as contact irritation, this reaction is dose dependent and is exacerbated by the fact that contact lenses slow clearance of the inciting agent.19 Most commonly, this reaction occurs when a contact lens wearer breaches protocol by not rinsing hydrogel lenses sufficiently after disinfection or enzyme treatment. The patient may also neglect hand washing after exposure to any number of household chemicals before handling the lenses. These reactions will respond quickly to discontinuing lens wear and avoiding the inciting agent. Cool compresses and preservative-free artificial tears will provide symptomatic relief during recovery. Severe cases may require a short course of corticosteroid drops, though some authorities observe that treatment fails to hasten resolution of the inflammation. If the wearer has “sensitive” eyes, conjunctivitis may occur because of preservatives in contact lens solutions. Changing to hypoallergenic care solutions and preservative-free saline for storage will often eliminate this reaction. The use of daily disposable soft lenses will limit exposure to the chemicals of routine lens care as well. In these situations it is often prudent to recommend the use of heat disinfection because it is superior to the hypoallergenic chemical disinfectants, particularly against acanthamoeba. Reinforcing the basic elements of proper contact lens care is always important.


Generally, allergic conjunctivitis secondary to contact lens wear may be distinguished from contact irritation by the presence of severe itching and swelling. In both situations, the ocular findings of diffuse papillary conjunctivitis are indistinguishable. True allergic contact allergy may be proven by skin-testing potential allergens for characteristic delayed erythema and induration associated with cell-mediated immunity. An inciting hapten may be environmental, in which case the contact lens presents the hapten in concentrated form to an already inflamed conjunctiva. Certain contact lens solution components, particularly preservatives such as thimerosal, have been implicated as allergens. Patients with ocular irritation in the presence of thimerosal-preserved solutions have a high rate of positive skin patch tests to thimerosal.62 One may minimize the prevalence of allergic contact lens disorders by carefully screening patients for nonocular allergic symptoms and conditions.18

Allergic conjunctivitis must be distinguished from hay fever conjunctivitis, perennial allergic conjunctivitis, atopic keratoconjunctivitis, vernal conjunctivitis, and giant papillary conjunctivitis by careful history and ocular examination.19 Once the diagnosis has been made, identifying the inciting hapten allows effective counseling for avoidance. Changing to less allergenic solutions may be necessary in the absence of an identifiable allergen. Symptomatic treatment is the same as that for toxic conjunctivitis. Control of itching may be accomplished by using topical vasoconstrictors and antihistamines during the acute phase. Topical ketorolac (Acular) has been effective for the symptomatic relief of itching but does not improve local tissue engorgement as well as topical vasoconstrictors. Oral antihistamines and rarely topical corticosteroids may be needed for severe cases. Topical cromolyn sodium (4%) may be used for chronic recurrent cases but has largely been supplanted by Patanol, Alocril, and Zaditor.


Giant papillary conjunctivitis (GPC) takes its name from the large papillae that form on the upper tarsal conjunctiva in response to contact lens wear or the chronic presence of other ocular foreign bodies.63,64 No contact lens type has escaped association with this complication.40,59,65 The classic triad of pruritis, excess mucus, and contact lens intolerance coupled with giant papillae of the upper tarsal conjunctiva make the diagnosis (Fig. 1).58 As the disease process progresses, the conjunctiva coalesces and the papillae become flattened. Ptosis may also develop. The condition must be differentiated from vernal keratoconjunctivitis because both have similar clinical features.19 Vernal keratoconjunctivitis occurs in warm weather, in adolescent males, and in the absence of contact lens wear.19 Those with seasonal allergies are more likely to develop GPC with contact lens wear.64,66

Fig. 1 Giant papillary conjunctivitis.

The pathophysiology of GPC is believed to involve conjunctival reaction to protein deposits on the lens surface, but mechanical trauma may also contribute.63 The immunologic reaction in GPC is similar to that found in vernal keratoconjunctivitis, but tear histamine levels are significantly greater for vernal.67 Tear IgE levels are also elevated in GPC patients relative to disease-free contact lens-wearing controls.68

Rigid lens wearers are less likely than hydrogel lens wearers to develop GPC because they accumulate less protein and are more completely cleaned.35,64,65 Most PMMA lenses do not require enzyme cleaning, but gas-permeable lenses should be enzyme cleaned at least once per month if not more often. The enzyme that seems to create the least inflammation in these patients is papain.63 Heat disinfection is associated with an increased prevalence of protein deposition and should be replaced by cold disinfection, preferably a hydrogen peroxide system.36,63

Treatment consists of discontinuing lens wear and initiating pharmocologic therapy with topical cromolyn sodium (4%) four times per day.63,69,70 Because the commercial preparation has shown stability problems and is no longer available, the solution must be made fresh for each patient every month. Promising data on symptomatic improvement with topical nonsteroidal anti-inflammatory agents leave hope for a new commercial preparation for this condition.71 Newer mast-cell stabilizers such as Patanol, Zaditor, and Alocril show promise for treating GPC but have not been widely tested.64 Topical corticosteroids are of little benefit in this disorder. Topical antihistamines and vasoconstrictors are valuable during the acute phase, which lasts 3 to 5 days in the absence of contact lenses. After resolution of itching, hyperemia, and mucus production, contact lenses may be refit and mast cell stabilizers used with them in place.63,64 Rigid gas-permeable lenses have often been recommended to replace hydrogel lenses because of their tendency to bind less protein.63,64 Others recommend new, clean soft lens use with reinforcement of appropriate lens care and frequent replacement or the daily use of a disposable soft lens.72,73 Chronic recurrent GPC requires permanent cessation of lens wear.


Contact lens-related superior limbic keratoconjunctivitis (CL-SLK) is a condition characterized by superior bulbar conjunctival inflammation, redundancy, and thickening associated with irregular superior corneal epithelium and an underlying V-shaped, faint, subepithelial, corneal opacity extending toward the center of the cornea. The condition is usually bilateral and symmetric. In noncontact lens wearers with SLK, hydrogel contact lens wear may be therapeutic. CL-SLK may be distinguished from its de novo counterpart by the pattern of punctate epithelial keratopathy (PEK) associated with each. A contact lens wearer develops PEK superiorly and extending down the peripheral cornea to the inferior one-third; whereas, the other form of SLK has PEK limited to the superior pole of the corneal epithelium. Contact lens wearers who develop this condition are often rigid lens wearers who switched to soft lenses or soft lens wearers who switched from heat disinfection to chemical.74 In each case preservative exposure is the presumptive cause, and a significant percentage show hypersensitivity to thimerosal.74,75 The majority of patients improve to baseline without lens wear over periods ranging from 1 week to 1 year. Corticosteroids and other traditional pharmacologic agents used to treat immunologic ocular diseases are largely ineffective in this condition. Some patients may return to lens wear using preservative-free solutions and heat disinfection.74

Pyogenic Granuloma

Pyogenic granuloma is rarely associated with contact lens wear. Two cases have been reported in which daily and extended lens wear is associated with formation of pyogenic granuloma.76,77 Both patients underwent excision of the mass with pathologic diagnosis. One lesion showed numerous foreign bodies embedded in the center.77 Follow-up information was available on one person only, who was able to return to lens wear by switching to rigid gas-permeable lenses.76

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The corneal epithelium bears the brunt of mechanical trauma and chemical alterations meted out during contact lens wear. Hypoxia is emerging as a major force in corneal epithelial damage not explainable by direct trauma related to lens defects or handling. Decreasing dK in rigid lenses in an animal model increased the observed degree of corneal epithelial cell swelling and desquamation.78 Extended soft contact lens wear has been implicated in specular microscopic observations of enlarged surface epithelial cells, suggesting a slower turnover of cells under these conditions.79 Even scant concentrations of common contact lens disinfectants, which come into intimate contact with the epithelial surface on a daily basis in hydrogel lens wear, cause epithelial cell retraction and decreased mitotic activity.80 The spectrum of corneal epithelial injury secondary to contact lens wear extends from mild punctate epithelial keratopathy in specific patterns to severe ocular surface disorders with indolent ulceration, anterior stromal scarring, superficial vascularization, and decreased vision requiring surgical intervention.81 There has even been a report of intraepithelial neoplasia associated with contact lens wear in the setting of extensive acute ultraviolet radiation exposure.82 Because isolated trauma to the epithelium may lead to serious corneal scarring, persistent contact lens abuse may lead to visual loss requiring penetrating keratoplasty.83,84 With enough foresight most contact lens wearers may avoid these devastating results.


Punctate epithelial keratopathy (PEK), or superficial punctate keratitis (SPK) to which it is often incorrectly referred, may result secondary to trauma, hypoxia, drying, chemical toxicity, or any permutation of the previous list.9,85 Discontinuing lens wear, eliminating potentially toxic topical medications, and treating tear surface abnormalities are the mainstays of therapy for these findings. Specific changes in contact lens material, fit, care, or wearing time may be required to prevent recurrence.

Contact lens overwear produces a coarse central pattern of staining that is often associated with excessive rigid and soft contact lens wear as well as with flat-fitting rigid lenses.9 The severity of staining is proportional to the duration of contact lens abuse and will determine recovery time following discontinuing lens wear. Discontinuing extended wear, decreasing daily wear time and refitting with steeper rigid lenses are all possible approaches to prevent recurrence.26 The presence of an arcuate patch of PEK near the superior limbus is suggestive of hypoxia secondary to a tight upper lid.9 This may be addressed by refitting with higher dK lenses or decreasing the duration of continuous lens wear.

Contact lens-related superior limbic keratoconjunctivitis presents with additional signs and symptoms to accompany the irregular superior PEK that develops in noncontact lens-related SLK.9,74,75 The diagnosis and treatment of this condition have been discussed previously under conjunctival complications.

Corneal PEK secondary to solution toxicity commonly presents as a diffuse pattern of superficial punctate fluorescein staining involving the entire corneal surface, often including the limbal conjunctival surface as well.9 Patients complain that the lenses sting immediately upon insertion. Review of lens care protocol is critical to eradicate this complication. Hand washing should be doubly stressed.

Dendriform punctate epithelial keratopathy occurs in the setting of severe contact lens solution toxicity or hypersensitivity.9,86–88 These dendriform lesions are slightly raised epithelial plaques that stain lightly with fluorescein (Fig. 2). In contrast, dendrites related to herpes simplex keratitis are intensely staining true ulcers and exhibit terminal bulbs. An association with contact lens solutions preserved with thimerosal and chlorhexidine has been suggested. Lens discontinuation and supportive therapy with nonpreserved tears and ointments constitute effective therapy. Lenses may be reintroduced using nonpreserved saline and thermal disinfection. Significant delay in diagnosis or persistent lens wear, in spite of these findings, may result in permanent stromal scarring beneath the dendriform epitheliopathy. Treatment with antivirals is not helpful and may worsen subsequent subepithelial scarring.

Fig. 2 Contact lens-induced dendriform keratitis.

Foreign body patterns of epithelial staining are similar to those seen with embedded foreign bodies in the upper tarsal conjunctiva. Contact lenses must be carefully inspected for embedded foreign bodies, tears, or nicks. Trapped debris under the lens is more commonly associated with rigid lens wear and may also cause this staining pattern. This finding may be avoided by attending to cleanliness at the time of lens insertion, avoiding contact lens wear for activities involving airborne foreign material, and controlling the amount of makeup applied to the lid margins.

Three and nine o'clock staining occurs commonly with rigid lens wear but may occur with soft lens wear as well.9 Pie-shaped wedges of PEK appear at the nasal and temporal limbus as a result of poor wetting of the local epithelium. Patients with pronounced against-the-rule astigmatism are more susceptible to this type of staining because of the bearing pattern of the lens. Persistent lens wear, in spite of this staining, may result in scarring and rarely pseudopterygia formation.89 Susceptible patients may develop raised scarring consistent with Salzmann's nodular degeneration. Refitting smaller diameter lenses with thinner edge design may eliminate mechanical trauma related to friction from the lens edge. Cases in which astigmatism is contributory may be addressed by using back-toric lens designs or soft-lens piggyback systems.

Inferocentral patches of PEK occur secondary to desiccation associated with contact lens- related dry eye or exposure. Supplemental lubrication during lens wear may be required to prevent recurrence. Decreasing wear time or switching to low water content, soft lenses may also improve results. Contact lens wear may be salvaged by permanent punctal occlusion in selected cases of aqueous deficiency dry eye. Topical cyclosporin-A drops (Restasis) may be used to restore enough tear production to allow continued lens wear.

Punctate epithelial keratopathy is a common finding often neglected as minor in the grand scheme of complications related to contact lenses. Remember that persistent epithelial staining puts the wearer at risk for microbial keratitis and may, when it progresses to coarse punctate erosions, represent the early stages of pseudomonas or acanthamoeba keratitis.90–92


Corneal abrasions may be caused by lens defects or may occur during lens insertion or removal. Abrasions occur more frequently with rigid lens wear because lens defects have sharp edges and foreign material gains access to area under the lens more easily.6 Corneal abrasions with soft lens wear are seen most frequently with tight lenses or extended wear lenses. In these situations acute epithelial hypoxia impairs epithelial attachment to Bowman's layer. Treatment is the same as that for noncontact lens-related abrasions. Careful examination of the lens and its fit and queries to the patient regarding techniques of lens removal are important to identify causes of recurrent abrasions.


Extended wear soft contact lenses are often used as a therapeutic modality for recurrent erosions resistant to medical therapy with topical hypertonic saline. However, animal studies suggest that extended contact lens wear worsens epithelial adhesion.93 This may explain the occasional contact lens intolerance seen with anterior epithelial basement membrane dystrophies.94 The osmotic effects of high water content, ultra-thin soft bandage lenses may counteract the effect of decreased adhesion by dehydrating the epithelium; however, this desiccation may, in turn, promote the formation of coarse punctate erosions in the central and paracentral cornea.9 These erosions are less likely to occur under highly humid conditions. Epithelial erosions related to extended contact lens wear elevate the risk of pseudomonas keratitis and should be treated accordingly.95


There are two distinct types of epithelial wrinkling, both of which are considered benign and non-progressive.9 The first type, called anterior corneal mosaic, may be induced in normal eyes by applying pressure externally or reducing intraocular pressure. This mosaic pattern occurs in association with rigid lenses that have significant central bearing, such as those fit for apical bearing in keratoconus.96 The pattern quickly resolves with removal of the lens but may persist in the presence of abnormally low intraocular pressure. The second type of wrinkling produces criss-crossing furrows on the epithelial surfaces that pool fluorescein.9,97 Extended wear, ultra-thin soft contact lenses are implicated as the cause of these furrows, which are deeper and fade more slowly than those related to rigid lens wear. Corneal wrinkling, also referred to as the “rippling phenomena,” is not associated with progressive changes of the corneal surface and does not necessitate lens removal.97

Air bubbles trapped beneath rigid lenses between blinks will form small indentations in the epithelial surface called dimples.9 Dimpling occurs in PMMA lens wearers most frequently but can rarely be found in soft lens wearers. No treatment is required.

Persistent pressure of the edge of a rigid lens may leave an arcuate furrow or ring on the corneal surface.9 This lens edge imprint typically lies inferior in the cornea but may represent the entire lens. Entire lens imprints are more commonly found with PMMA lenses and extended wear, gas-permeable, rigid lenses that adhere to the corneal surface during sleep.37,38 Recurrent lens imprints may result in corneal distortion that over time may become permanent. Further discussion of the implications and treatment of corneal distortions related to contact lens wear will be addressed in the section entitled “Corneal Deformation: Corneal Warpage and Keratoconus.”


Epithelial microcysts form in response to the hypoxia of soft contact lens wear.9,98–100 They appear after 6 to 8 weeks of lens wear and appear as translucent dots that show reversed illumination when viewed in retroillumination. They may be confused with lesions found in Meesmann's epithelial dystrophy but will resolve with proper care. The prevalence and severity are inversely proportional to lens dK and proportional to lens wearing time. Altering either of these parameters in a patient who has developed greater than 50 microcysts or whose cysts begin to stain with fluorescein will cause gradual reduction of the number of microcysts within 3 months. Rarely lens wear must be discontinued.


Superficial corneal neovascularization is a response to persistent hypoxia secondary to contact lens wear (Fig. 3).9,101–103 Rigid lenses rarely develop limbal hyperemia greater than normal controls. Daily wear–lens patients will often show an apparent increase in limbal vascularization, which actually represents limbal capillary dilation and rarely progresses to frank neovascularization. Extended-wear soft contact lens wearers most often exhibit significant limbal new vessel growth. Topical nonsteroidal antiinflammatory agents may suppress neovascularization, but their use has not become routine.104 Most often treatment consists of changing from extended to daily wear schedules, fitting with higher dK or thinner lenses or fitting with a looser soft lens. The use of soft extended wear lenses after penetrating keratoplasty is particularly risky because of the rapid neovascular response observed.105

Fig. 3 Severe superficial corneal neovascularization.


Corneal hypoesthesia is most commonly associated with PMMA contact lens wear.9,106 This complication explains the blissful ignorance of some more severe complications by the average PMMA lens wearer. Refitting with gas-permeable rigid lenses restores corneal sensitivity of these patients within 2 to 3 weeks.107 Soft contact lens wear has been implicated in corneal hypoesthesia to a degree less than PMMA lens wear, and the hypoesthesia is inversely proportional to the oxygen transmissibility of the lens.9,108 Corneal hypoesthesia contributes to the osmotic effects of contact lens wear by decreasing reflex tear secretion.9

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Corneal hypoxia leads to accumulation of lactate in the stroma.9 The presence of increased stromal levels of lactate increases the osmotic pressure within the stroma, and edema ensues.108 There is good evidence that the attendant stromal acidosis impairs endothelial cell function, which in turn exacerbates stromal swelling.109 Corneal stromal edema results in corneal thickening, stromal striae and folds, corneal distortion, and increased light backscattering secondary to disruption of the regular pattern of collagen lamellae.9,110,111 The edema may be irreversible in eyes in which the endothelium is severely compromised.112 Rarely with modern lenses epithelial edema, or Sattler's veil, produces glare and halos around bright lights.111 Because stromal thinning is noted with long term soft lens wear, swelling in these patients may only bring the corneal thickness into the normal range.9

The minimum oxygen transmissibility of a contact lens required to prevent edema both in the open- and closed-eye situations may be calculated experimentally.113,114 Clinically, however, there is a significant intersubject variability in edema thresholds for the same lens material and thickness.115,116 To provide a safe margin for the vast majority of the lens wearing population, it is important to maximize the oxygen transmissibility of contact lenses, particularly those for extended wear.117 In some cases cessation of extended lens wear is necessary to avert recurring bouts of blurred vision upon awakening. Persistent stromal edema over time may have adverse effects on corneal endothelial cells, a subject to be discussed later in this chapter.


Corneal hypoxia related to contact lens wear may induce deep stromal neovascularization in both rigid and soft lens wearers.9,118 In rigid lens wearers, PMMA use is a significant risk factor. Low oxygen permeable and thick (i.e., aphakic) soft lenses are more likely to cause this response.119,120 Eyes that have suffered surgical trauma are also at risk.9,119 Cessation of lens wear, reduction in wearing time, or change to lenses with higher dK/L values slow or halt the progression of neovascularization. More creative treatment involves exposure of the ocular surface to increased concentrations of oxygen.118 The vessels will not recede but shrink to form “ghost vessels.”

Complications related to stromal neovascularization are rare and include intrastromal hemorrhage and interstitial keratitis.9 Intrastromal hemorrhage most commonly occurs in the setting of aphakic, extended, soft lens wear but has been reported with daily cosmetic lens wear as well.121–123 The hemorrhages clear leaving varying degrees of attendant visual loss, and at least one patient required corneal transplantation to restore vision.122 Circinate-pattern lipid exudate surrounding stromal vessels has been described in a group of five daily soft lens wearers.124 These infiltrates differ from classic interstitial keratitis because they did not increase with time, were not associated with an inflamed eye, and did not respond to topical corticosteroids.


Stromal opacities may be seen with or without concomitant stromal vascularization.9 In contrast to superficial, deep stromal vascularization more commonly results in permanent corneal scarring. Superficial stromal opacities rarely occur in association with generalized superficial ocular inflammation, but recovery from the causal insult generally precedes dissolution of stromal scarring.125 An unusual arcuate superficial stromal opacity of the superior cornea has been reported in a small group of soft, cosmetic, daily lens wearers.126 The opacities were felt to result from tight eyelids, although a case could be made for the type of lens as cause.127 Most anterior stromal opacities are associated with soft lens wear, except for those found in keratoconus, which may occur both with and without contact lens wear. Keratoconus patients most likely to develop stromal opacities are those fit with large flat lenses instead of small lenses with apical clearance.128

Deep stromal opacities have been reported in association with both rigid and soft lens wear.129 These whitish, pre-Descemet's opacities form bilaterally in the central corneas of long-term contact lens wearers and are associated with marked endothelial polymegathism. In some cases the opacities may cause visual loss but will gradually disappear with cessation of lens wear or change to a more oxygen permeable lens. With the different types of superficial opacities and deep stromal opacities, thimerosal toxicity, allergy, and chronic hypoxia have been implicated as potential causes.9,125–129


Sterile corneal infiltrates associated with contact lens wear are generally multiple, small, anterior stromal infiltrates found most often at the corneal limbus but also in clusters in the central cornea (Fig. 4).130–132 Rarely the epithelium alone may be involved and is commonly intact over stromal infiltrates. The anterior chamber may show mild to severe cellular reaction.130 Corneal infiltrates related to extended soft lens wear tend to form near the superior limbus.133 These infiltrates must be distinguished from their infectious counterparts, including chlamydia, by careful historical consideration and clinical examination.131 If there is any doubt regarding the etiology of the infiltrates, scrapings for stain and culture should be taken, followed by appropriate broad-spectrum topical antibiotic therapy.

Fig. 4 Twelve o'clock sterile marginal corneal infiltrate.

Using rigid gas permeable lens wear as the referent, soft lens wearers and particularly extended soft lens wearers carry a significantly higher risk of developing sterile infiltrates.6,9,130,134 PMMA lens wearers are the least likely to suffer this complication.134 A longer duration of soft lens wear provides a proportionately increased risk of developing these infiltrates.132,135 The rate of sterile infiltrates per year for disposable extended soft lens wear in a prospective study was as high as 7%, suggesting that disposable lenses are not the solution to this problem.136 Daily disposable soft lenses or soft silicone hydrogel lenses afford the lowest rate of peripheral infiltrates for soft lens wear.22,132

Various theoretic causes include chemical hypersensitivities to thimerosal and chlorhexidine, exposure to a variety of environmental toxins through digital contamination, improper enzyme use, staphylococcal lid disease, and bacterial contaminants of contact lens cases.130,137 Antigenic debris held chronically against the corneal surface has been cited as a potential basis for sterile infiltrates, particularly with extended soft lens wear.130–134

Required therapy consists of discontinuing lens wear and treating cautiously with topical corticosteroids, a practice that necessitates frequent initial examinations.130 Lens wear should cease until there is complete resolution of all infiltrates and adequate corticosteroid taper. Recurrences may be avoided by careful review of contact lens care and handling, cessation of suspected offending chemicals, insistence on clean contact lens cases and treatment of any associated staphylococcal lid disease. Recurrent infiltrates associated with extended soft lens wear may require the use of soft or rigid daily wear lenses. Daily disposable and silicone hydrogel soft lenses are an excellent strategy for prevention in susceptible individuals. The prognosis for the majority is good, with visual loss remaining rare.


Infectious keratitis is the single most feared complication of contact lens wear.138 Corneal infections may range from small peripheral ulcers to large suppurative central ulcers. Infectious ulcers must be differentiated from sterile ulcers, particularly in association with disposable extended lens wear. Bacterial keratitis occurs most frequently in association with extended soft contact lens wear and least frequently among rigid PMMA wearers. Bacterial keratitis is by far the most frequent form of infectious keratitis associated with contact lens wear, with Pseudomonas aeruginosa being the most frequent isolate (Fig. 5). In most cases of infectious keratitis, there is an identifiable breach of contact lens care protocol that predisposes the patient to infection. It is imperative to make a swift and accurate diagnosis of infectious keratitis and to initiate appropriate topical antibiotic therapy to minimize visual loss secondary to stromal scarring.

Fig. 5 Central Pseudomonas keratitis with hypopyon.

The epidemiology of infectious keratitis associated with contact lens wear has been extensively examined over the past 15 years.20,139–158 A survey of ophthalmologists and households in New England produced estimates of the annual incidence of infectious keratitis associated with cosmetic extended (20.9 per 10,000 persons) and daily (4.1 per 10,000 persons) contact lens wear.139 The same study group estimated the annual incidence of infectious keratitis among aphakic contact lens wearers to be 52 per 10,000 persons and significantly higher for those who practiced extended wear.141 With estimates of 9 million daily lens wearers and 4 million extended lens wearers, this incidence translates to 12,000 new cases of infectious keratitis related to cosmetic soft contact lens wear annually in the United States alone.140,141 The relative risks of infectious keratitis with extended versus daily wear reveal that risk rises incrementally with the duration of extended wear.140 Advances in soft, silicone, hydrogel materials have reduced complications for extended wear, but the newer lenses have not been compared to older lenses in a large study of complication rates.22 Compared to daily contact lens wear, extended wear on a routine basis carries a 10 to 15 times increased risk of infectious keratitis.140 In addition, the risk for soft cosmetic daily wear exceeds that for daily rigid gas permeable lens wear.158 Daily disposable soft lens wear may afford the best strategy to avoid infection.31–33

Contact lens-related keratitis as a proportion of all cases of infectious keratitis ranges from 11% to 44% as reported in the literature.142,143,148,151,154–156 The trend over the past 15 years has been for the proportion to increase, a trend that parallels the increasing popularity of contact lens wear and particularly extended wear.147,149,151,153 Contact lens-related keratitis occurs most frequently with aphakic and cosmetic soft extended lens wear.142,147 This observation would support the finding that young myopes and old aphakes tend to carry the highest risk for infection.147 Smoking introduces an increased risk of keratitis for all lens types.150 Failure to follow appropriate lens-care protocols increases the risk of infectious keratitis.4,144 Occlusion and corticosteroid use are associated with more severe ulceration.146,148 Contact lens-related corneal ulcers tend to occur more frequently during the summer months (51% in one study) when contact lens wearers are more active, particularly in water sports.157

The prevailing frequency of organisms isolated from cases of contact lens-related infectious keratitis will dictate the appropriate choice of broad-spectrum topical antibiotic therapy prior to receiving results of ocular cultures. Compared to other causes of corneal ulcers, contact lens wear is more often associated with gram-negative infection and particularly with infection by P. aeruginosa.142,143,145,148,149,151,153 The increased prevalence of pseudomonal infections may have its basis in the preferential binding of pseudomonas to soft contact lenses.36,159 Staphylococcal and streptococcal species are a close second and third in most studies.142,145,151 The order is reversed for bandage contact lenses, which tend to be contaminated by common conjunctival commensals and gram-positive organisms.154 More polymicrobial infections are found with bandage lens wearers than with their cosmetic counterparts.145,160 Gram-negative infections cause the most morbidity after final outcome.

Careful examination followed by cultures from the ulceration is the standard of treatment for any stromal keratitis suspected to be infected. Complete descriptions of protocols and techniques for taking samples for stains and cultures may be found in the chapter devoted specifically to infectious keratitis. The use of frequent topical ciprofloxacin (0.3%) or fortified tobramycin (14 mg/mL) will give good coverage for most bacteria associated with contact lens wear. Despite current evidence for the use of ciprofloxacin as a single drug in the treatment of bacterial keratitis, most authorities recommend the addition of a fortified cephalosporin (cefazolin 50 mg/mL) to the regimen to provide additional coverage for gram-positive organisms that are showing increasing resistance to ciprofloxacin. The streptococcal species, in particular, are difficult to treat.161 The availability of fourth generation fluoroquinolones (moxifloxacin and gatifloxacin) has begun to change recommendations regarding single-drug therapy. Alternating the two medications every ½-hour should be performed around-the-clock until clinical improvement is documented. Admission to the hospital is optional and is based on the practitioner's assessment of potential compliance under such difficult circumstances. The use of corticosteroids should be avoided arguably until epithelialization is complete or until one identifies a susceptible organism and documents clinical improvement. Corticosteroids should be used with extreme caution in cases of infectious keratitis of unknown etiology, which fail to respond to initial therapy. These cases are at high risk to be fungal or parasitic infections, which are discussed later in this chapter.

The association of contact lens-related corneal infections with breaches in contact lens care protocols provides impetus and direction for teaching each contact lens wearer the techniques that are most protective against infection.4,144 Many contact lens wearers, particularly those with more than 2 years of contact lens wearing experience, are noncompliant with appropriate care routines.1 In one study an estimated 90% of contact lens wearers who suffer an episode of infectious keratitis have inadequate contact lens care, a contaminated contact lens case, contaminated solutions, or any combination of these three.162 Extended-wear contact lens wearers are particularly likely to have old and contaminated solutions.162 The contamination of contact lens storage cases can be a significant risk factor for infectious keratitis, and regular cleaning of the case has a protective effect.150,163 Despite regular cleaning and disinfection, contact lens cases may be colonized by resistant bacteria, particularly Bacillus species, and may require routine disposal. Chemical disinfection, though popular, is generally less effective than heat disinfection.138 The hydrogen peroxide systems appear to combine the most bacterial killing with the least toxicity, if used correctly.138 The “one-step” hydrogen peroxide systems lack some of the killing efficacy of the other solutions because exposure time is limited.164 Enzymatic cleaning weekly is important for both daily and extended wear lenses because protein deposits enhance bacterial adherence to the lens surface.36,165 Careful training of each new contact lens wearer with regard to appropriate lens care is vital to preventing infectious keratitis. The protocols for lens handling, cleaning, disinfection, enzyming, and storage must be stressed at each return visit for every contact lens wearer regardless of experience. Patients who demonstrate a persistent inability to follow appropriate lens care should be advised to switch to daily disposable or silicone hydrogel soft lenses.

Particular attention has been paid to the issue of infectious keratitis related to the use of soft extended wear contact lenses.166–170 The relative convenience of extended wear, particularly for aphakic eyes and high refractive errors, has resulted in a dramatic increase in the number of patients wearing soft contact lenses while sleeping. Initially the rationale for extended wear was to decrease lens manipulation, which would translate to a decrease in the rate of bacterial lens contamination and infectious keratitis. As mentioned previously, the opposite has proved to be the case. Punctate epithelial keratopathy (PEK), which was discussed previously in this chapter as a characteristic of overwear of extended-wear soft contact lenses, is also associated with a higher yield of positive cultures for bacteria, pseudomonas in particular.90 Coarse PEK may even represent a forme fruste of pseudomonal keratitis with extended lens wear.91 Animal studies have shown that extended contact lens wear increases corneal epithelial binding of pseudomonas three to eight times.171 Even disposable soft lenses, which were expected to protect against lens handling-induced bacterial keratitis, show increased binding of pseudomonas with wearing time of less than 7 days.172 As experience with disposable lenses grows and their use increases, the risk for infectious keratitis has been found to be at least equal to if not greater than that for conventional extended soft lens wear.151,173,174 One exception may be that for the highly oxygen permeable soft silicone hydrogel lenses.22 The evidence points to the degree and duration of hypoxia as the most important risk factor for developing infectious keratitis secondary to contact lens wear. The patient who requests extended wear lenses of any kind should be warned of the increased risk for infection, counseled to remove the lenses for any ocular injection or discomfort and entreated to seek ophthalmologic care, if the symptoms fail to resolve within 24 hours or worsen after removal.


Fungal keratitis is a rare but important complication of contact lens wear. It occurs in approximately 3% to 4% percent of total cases of infectious keratitis related to cosmetic lens wear but is found more frequently with therapeutic lens wear.154,156,175 Indolent ulcerations responding poorly to initial therapy and associated with dense, fluffy stromal infiltrates with feathery margins are likely to be fungal infections despite negative stains and initial cultures. Satellite lesions are commonly seen as well as endothelial placques behind the stromal infiltrate.138 There is usually mild to moderate anterior chamber reaction. Fungal elements on initial smears are an indication for initiating treatment with topical antifungal agents like natamycin (5%). However, one may have to wait for culture results of not only the lesion, but also the contact lens case and contact lens. Fungal growth may actually be found in soft contact lenses without an associated keratitis.176–178 These lenses should be replaced and the source of contamination investigated by reviewing carefully the patient's lens care routine. The full spectrum of fungal keratitis diagnosis and treatment is beyond the scope of this chapter and is discussed in detail elsewhere in these volumes.


Acanthamoeba keratitis is a devastating but fortunately rare complication of contact lens wear.92,138,179–184 Infections have been reported with all lens types but tend to occur most frequently with soft lens wear. Recently, even disposable lenses have been implicated.183 Of the 18 studies examining infectious keratitis in contact lens wearers cited for this chapter, only 2 mention cases of acanthamoeba keratitis, amounting to much less than 1% of all the cases compiled.151,154 Many of the initial cases were traced to the use of distilled water and saline tablets to rinse and store soft contact lenses. With the attention paid to the early cases and their causes, the prevalence has begun to drop.

The key to effective treatment of acanthamoeba keratitis is early diagnosis, because once it has penetrated into the stroma, medical therapy is much less effective. Early signs include a dendriform keratitis, diffuse coarse punctate epithelial keratopathy, or elevated epithelial lines with patchy epithelial and subepithelial infiltrates.92,138 Radial keratoneuritis has been said to be pathognomonic for the disease but occurs in few cases.138 Medical therapy with topical neomycin and propamidine isethionate (Brolene), with or without oral ketoconazole, has a good chance for success early in the course of the disease.138,184 If the diagnosis is made when only epithelial disease is present, wide debridement of the affected area is quite helpful. Many cases in which the diagnosis is delayed require therapeutic keratoplasty, which has a poor prognosis and reinfection rates estimated at one-third.138,184 A more complete discussion of the diagnosis and treatment of acanthamoeba keratitis may be found elsewhere in these volumes.

One should screen contact lens patients with keratitis for contact lens care practices that put them at risk for exposure to acanthamoeba. The patient will usually admit to using nonsterile solutions at some point in lens care. A history of lengthy exposure to dust or fresh water (lake or stream more than tap) should heighten the level of concern for acanthamoeba. In cases of acanthamoeba keratitis related to contact lens wear in which there is no obvious contaminated source, careful examination of lens solutions will usually reveal contamination with trophozoites or cysts. Many currently available and popular contact lens solutions, cleaners, and disinfectants are not effective at either killing acanthamoeba cysts or preventing the growth of the trophozoites.185–187 Some effective disinfectants cited in these studies, as well as some effective single preservative agents include: chlorhexidine 0.001%, poliaminopropyl biguanide 0.0015%, benzalkonium chloride 0.001%, hydrogen peroxide 3%, and a combination of thimerosal 0.004% and EDTA 0.1%.186


Deformation of the cornea by contact lens wear occurs almost exclusively with rigid lens wear, but has been reported in association with soft contact lens wear as well.188–193 The causal relationship between contact lens wear and keratoconus has been debated in the literature, but no definitive proof exists that contact lens wear results in corneal ectasia consistent with keratoconus in patients who would not have otherwise developed the condition.194–196 In the past, knowing which patients being fitted with contact lenses for the first time had early keratoconus was next to impossible. With the advent of computer generated corneal topographic maps, keratoconus may be diagnosed prior to the development of pathognomonic biomicroscopic signs, such as Fleischer's iron ring, Vogt's striae, and cone formation with thinning. With corneal topography, subtle changes in corneal shape have been identified in “normal” contact lens wearers, both soft and hard.188 This new technology allows for the design of a clinical trial to screen for early keratoconus in potential contact lens wearers and in turn to randomize between spectacle and contact lens correction. The epidemiology of both corneal warpage and keratoconus related to contact lens wear strongly suggests that some corneas are susceptible to corneal ectasia because of unidentified defects in the collagen matrix that are activated by either mechanical or hypoxic forces of contact lens wear.192,194–196

Both corneal warpage and keratoconus present with the clinical course of frequently changing refractions requiring frequent contact lens refitting. During the time of frequent refitting, spectacle correction results in increasingly poor visual acuity. Keratometric mires become increasingly irregular and steep. The degree of corneal astigmatism may increase, decrease, or remain unchanged. Corneal topography is particularly helpful early to distinguish between keratoconus and corneal warpage. Decentration of the lens noted prior to topography most often predicts the area of flattening in patients with corneal warpage.191,193 Patients with keratoconus have a characteristic inferior steepening in a discrete area. In contrast, corneal warpage may present with a variety of irregular topographic patterns. Most frequently there is central irregular astigmatism, loss of radial symmetry, and loss of the usual pattern of progressive flattening toward the periphery.193

The hallmark of corneal warpage is improvement observed following cessation of lens wear. Inferior steepening in keratoconus will not change pattern significantly, but the topography of a patient with corneal warpage will change with each visit. Although many patients with corneal warpage return to regular mires in recovery periods ranging from several weeks to almost 1 year, there are some who suffer permanent irregular astigmatism secondary to long-term rigid lens wear. Generally, the risk for corneal warpage is greatest for PMMA lens wearers and increases with duration (both daily and in total years) of lens wear.189,190 Though poor lens fitting is a risk factor, corneal warpage may occur despite optimal fitting of rigid lenses. The risk of corneal warpage dampens the enthusiasm for using rigid lenses to correct myopia using orthokeratology.

For situations in which the diagnosis is in question, a trial of several weeks without lens wear will help to uncover corneal warpage that happens to mimic the topographic pattern of keratoconus.193 Patients with keratoconus must continue contact lens wear unless spectacle correction is adequate. Despite cessation of lens wear the condition is likely to progress to varying degrees that are, for the most part, unpredictable. Corneal warpage responds to cessation of lenses in most cases within 3 to 4 weeks, but recovery may extend to 6 months or more in severe cases.189,190,193 Some corneas never resume a regular or consistent shape. In patients with poorly fitting lenses, refitting may be all that is required. PMMA lens wearers may be successfully refit with gas-permeable lenses. Toric soft lens fitting is another alternative for both PMMA and gas-permeable wearers who develop corneal warpage. During the period of recovery and refitting, the patient must understand that frequent changes in contact lenses or spectacles may be required to keep pace with changing topography and to provide useful vision. Patients who exhibit persistent topographic changes despite refitting should not continue to wear contact lenses.

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A combination of hypoxia and hypercapnia results in stomal acidosis to which corneal endothelial cells are susceptible.9,197 Reversible endothelial blebs and irreversible endothelial cell polymegathism and pleomorphism have been reported with every lens type, occurring most frequently with extended lens wear, low oxygen permeable lenses, and many years of lens wear.


Corneal endothelial cell blebs are focal, circumscribed defects in the endothelial mosaic that represent edematous endothelial cells.9,197 They occur as a result of corneal hypoxia related to contact lens wear of any kind and are reversible within 30 minutes upon removal of the lens.197–200 The response occurs more readily in eyes unaccustomed to contact lens wear, suggesting some ability to compensate on the part of the endothelium. Endothelial blebs are not associated with any long-term sequelae but indicate relative corneal anoxia secondary to contact lens wear.


The effects of contact lens wear on the shape and number of cells comprising the corneal endothelium may be easily measured using the specular microscope. Significant increases in the mean variation in cell size (polymegathism) and cell shape (pleomorphism) have been frequently reported in specular microscopic studies of long-term PMMA wearers and has been documented with extended gas-permeable lens wear of only 3 months duration.199–202 Though most studies have shown no decrease in cell density related to contact lens wear, one study of unilateral PMMA wearers and another of keratoconus patients after corneal transplantation showed a decrease in mean cell density in the eye wearing the lens.203,204 Though there is a trend toward improvement after discontinuing lens wear, there remains no significant change up to 60 months after cessation of lenses.205

Endothelial cell changes have also been documented in soft contact lens wearers, despite the fact that soft lens wear was not common until at least a decade after PMMA lens wear became common.206–214 Though extended-wear lenses are more likely to be associated with polymegathism and pleomorphism, these changes have been documented with daily soft lens wear as well.207,208 In addition, fluorophotometric analysis of both hard and soft contact lens wearers shows an increased endothelial permeability, which correlates with impairment of the endothelial barrier function. Recent studies suggest that corneal edema and polymegathism in soft extended-wear patients are related.212 The lack of corneal edema found by comparing mean corneal thickness measurements of contact lens wearers and controls may be fallacious based on the tendency toward stromal thinning after many years of contact lens wear.9 Whether these endothelial changes carry any clinical significance, particularly with respect to endothelial cell loss during intraocular surgery, has yet to be proven. Nevertheless, there is enough evidence linking polymegathism and pleomorphism of the endothelium to endothelial cell dysfunction that patients should be warned of the potential future risks, particularly when wearing PMMA or extended-wear lenses. PMMA lens wearers should be strongly encouraged to switch to gas-permeable lenses.


As contact lens wear becomes more prevalent in our culture, there develops among wearers and prescribers a tendency to trivialize the risks involved with wearing them. Yet the risks remain real and persistent despite advances in contact lens quality and care. An increase in the popularity of extended wear may account for the relative stability of complication rates despite progress in lens quality and care. A lifestyle that demands extended wear lenses is less likely to allow cessation of lens wear until the eye can recover from the inevitable hypoxic, mechanical, or inflammatory incidents that threaten vision. The availability of highly oxygen permeable extended wear lenses and daily disposable lenses has lessened these unnatural stresses on the ocular surface. Also, the move toward laser refractive correction of ametropia is reducing the total numbers of contact lens wearers.

Contact lenses free those with ametropia from the limits imposed upon them by wearing spectacles. It is the primary responsibility of the contact lens prescriber to educate each lens wearer about potential side effects of contact lens wear, which may lead to loss of vision. If the prospective wearer understands the risks involved in wearing contact lenses and the relative risks for each type, only then may that person make the appropriate choice of therapy for his or her ametropia. No less important is the continuing education of experienced lens wearers about new developments in contact lens technology and the importance of religious lens care, despite years without serious complications. Finally, the contact lens prescriber must recognize the signs of chronic recurrent complications secondary to contact lens wear and help the wearer to accept other forms of correction.

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1. Chun M, Weissman BA: Compliance in contact lens care. Am J Optom Physiol Opt 64(4):274–276, 1987

2. Ky W, Scherick K, Stenson S: Clinical survey of lens care in contact lens patients. CLAO J 24(4):216–219, 1998

3. Smith SK: Patient noncompliance with wearing and replacement schedules of disposable contact lenses. J Am Optom Assoc 67(3):160–164, 1996

4. Dejaco-Ruhswurm I, Scholz U, Hanselmayer G, Skorpik C: Contact lens induced keratitis with contact lens wear. Acta Ophthalmol Scand 79(5):479–483, 2001

5. Zadnik K, Mutti DO, Cutter GR, Chalmers RL: The effect of refractive error on hydrogel contact lens-induced complications and patient self-management behaviors. Optom Vis Sci 78(9):652–656, 2001

6. Stapleton F, Dart J, Minassian D: Nonulcerative complications of contact lens wear: Relative risks for different lens types. Arch Ophthalmol 110:1601–1606, 1992

7. Genvert GI, Cohen EJ, Parlato CJ, et al: A prospective study of emergency room visits for contact lens related problems. CLAO J 13(1):42–45, 1987

8. Radford CF, Gastaldo-Brac V, Hill AR: Attendance of contact lens wearers at an ophthalmic accident and emergency unit. Ophthalmic Physiol Opt 18(1):63–65, 1998

9. Bruce AS, Brennan NA: Corneal pathophysiology with contact lens wear. Surv Ophthalmol 35:25–58, 1990

10. Quinn TG, Schoessler JP: Human corneal epithelial oxygen demand-population characteristics. Am J Optom Physiol Opt 61(6):386–388, 1984

11. Holden BA, Sweeney DF, Sanderson G: The minimum precorneal oxygen tension to avoid corneal edema. Invest Ophthalmol Vis Sci 25:476–480, 1984

12. Polse KA: Factors controlling oxygen tension under a hydrogel contact lens. J Am Optom Assoc 52(3):203–208, 1981

13. Stefansson E, Foulks GN, Hamilton RC: The effect of corneal contact lenses on the oxygen tension in the anterior chamber of the rabbit eye. Invest Ophthalmol Vis Sci 28:1716–1719, 1987

14. McNamara NA, Polse KA, Brand RJ, et al: Tear mixing under a soft contact lens: Effect of lens diameter. Am J Ophthalmol 127(6):659–665, 1999

15. Stefansson E, Wolbarsht ML, Landers MB: The corneal contact lens and aqueous humor hypoxia in cats. Invest Ophthalmol Vis Sci 24:1052–1054, 1983

16. Giasson C, Bonanno JA: Corneal epithelial and aqueous humor acidification during in vivo contact lens wear in rabbits. Invest Ophthalmol Vis Sci 35(3):851–861, 1994

17. Harvitt DM, Bonanno JA: PH dependence of corneal oxygen consumption. Invest Ophthalmol Vis Sci 39(13):2778–2781, 1998

18. Kumar P, Elston R, Black D, et al: Allergic rhinoconjunctivitis and contact lens intolerance. CLAO J 17(1):31–34, 1991

19. Ehlers WH, Donshik PC: Allergic ocular disorders: A spectrum of diseases. CLAO J 18(2):117–124, 1992

20. Dart JKG: Disease and risks associated with contact lenses. Br J Ophthalmol 77:49–53, 1993

21. Hardman Lea SJ, Neugebauer MAZ, Smith RG, Vernon SA: The incidence of ophthalmic problems in the contact lens wearing population. Eye 4:706–711, 1990

22. Nilsson SE: Bacterial keratitis and inflammatory corneal reactions: Possible relations to contact lens oxygen transmissibility: the Harold A. Stein Lectureship 2001. CLAO J 28(2):62–65, 2002

23. Dumbleton K: Noninflammatory silicone hydrogel contact lens complications. CLAO J 29(1 suppl):S186–S189, 2003

24. Lee KY, Lim L: Pseudomonas keratitis associated with continuous wear silicone-hydrogel soft contact lens: A case report. CLAO J 29(4):255–257, 2003

25. Yeniad B, Adam YS, Bilgin LK, Gozum N: Effect of 30-day continuous wear of silicone hydrogel lenses on corneal thickness. CLAO J 30(1):6–9, 2004

26. Rapkin JS: The effect of daily wear time on contact lens complications. CLAO J 14(3):139–142, 1988

27. Keech PM, Ichikawa L, Barlow W: A prospective study of contact lens complications in a managed care setting. Optom Vis Sci 73(10):653–658, 1996

28. Levy B, McNamara N, Corzine J, Abbott RL: Prospective trial of daily and extended wear disposable contact lenses. Cornea 16(3):274–276, 1997

29. Hamano H, Watanabe K, Mamano T, et al: A study of the complications induced by conventional and disposable contact lenses. CLAO J 20(2):103–108, 1994

30. Pritchard N, Fonn D, Weed K: Ocular and subjective responses to frequent replacement of daily wear soft contact lenses. CLAO J 22(1):53–59, 1996

31. Suchecki JK, Ehlers WH, Donshik PC: A comparison of contact lens-related complications in various daily wear modalities. CLAO J 26(4):204–213, 2000

32. Ilhan B, Irkec M, Orhan M, Celik H: Surface deposits on frequent replacement and conventional daily wear soft contact lenses: A scanning electron microscopic study. CLAO J 24(4):232–235, 1998

33. Solomon OD, Freman MI, Boshnik EL, et al: A 3-year prospective study of the clinical performance of daily disposable contact lenses compared with frequent replacement and conventional daily wear contact lenses. CLAO J 22(4):250–257, 1996

34. Bennett ES, Egan DJ: Rigid gas-permeable lens problem solving. J Am Optom Assoc 57(7):504–511, 1986

35. Fowler SA, Korb DR, Finnemore VM, Allansmith MR: Surface deposits on worn hard contact lenses. Arch Ophthalmol 102:757–759, 1984

36. Tripathi RC, Tripathi BJ, Silverman RA, Rao GN: Contact lens deposits and spoilage: Identification and management. Int Ophthalmol Clin 31(2):91–120, 1991

37. Kenyon E, Polse KA, Mandell RB: Rigid contact lens adherence: Incidence, severity and recovery. J Am Optom Assoc 59(3):168–174, 1988

38. Swarbrick HA, Holden BA: Rigid gas permeable lens binding: Significance and contributing factors. Am J Optom Physiol Opt 64(11):815–823, 1987

39. Poggio EC, Abelson M: Complications and symptoms with disposable daily wear contact lenses and conventional soft daily wear contact lenses. CLAO J 19(2):95–102, 1993

40. Poggio EC, Abelson M: Complications and symptoms in disposable extended wear lenses compared with conventional soft daily wear lenses and soft extended wear lenses. CLAO J 19(1):31–39, 1993

41. Lamer L: Extended wear contact lenses for myopes: A follow-up study of 400 cases. Ophthalmology 90:156–161, 1983

42. Weissman BA, Pearson TR: Clinical management of cosmetic extended-wear contact lens failure. J Am Optom Assoc 57(6):448–450, 1986

43. Holden BA, Swarbrick HA, Sweeney DF, et al: Strategies for minimizing the ocular effects of extended contact lens wear: A statistical analysis. Am J Optom Physiol Opt 64(10):781–789, 1987

44. Taylor DSI: Risks and difficulties of the treatment of aphakia in infancy. Trans Ophthalmol Soc UK 102:403–406, 1982

45. Graham CM, Dart JKG, Buckley RJ: Extended wear hydrogel and daily wear hard contact lenses for aphakia: Success and complications compared in a longitudinal study. Ophthalmology 93:1489–1494, 1986

46. Spoor TC, Hartel WC, Wynn P, Spoor CK: Complications of continuous-wear soft contact lenses in a nonreferral population. Arch Ophthalmol 102:1312–1313, 1984

47. Hayworth NAS, Asbell PA: Therapeutic contact lenses. CLAO J 16(2):137–142, 1990

48. McDermott ML, Chandler JW: Therapeutic uses of contact lenses. Surv Ophthalmol 33:381–394, 1989

49. Ong BL, Larke JR: Meibomian gland dysfunction: Some clinical, biochemical and physical observations. Ophthalmic Physiol Opt 10(2):144–148, 1990

50. van den Bosch WA, Lemji HG: Blepharoptosis induced by prolonged hard contact lens wear. Ophthalmology 99:1759–1765, 1992

51. Epstein G, Putterman A: Acquired blepharoptosis secondary to contact-lens wear. Am J Ophthalmol 91:634–639, 1981

52. Bellan L, Buffam F: The ‘O’ sign-clue to a lost lens. Can J Ophthalmol 25(7):348–350, 1990

53. Jones D, Livesy S, Wilkins P: Hard contact lens migration into the upper lid: An unexpected lump. Br J Ophthalmol 71:368–370, 1987

54. Sebag J, Albert DM: Pseudochalazion of the upper lid due to hard contact lens embedding-case reports and literature review. Ophthalmic Surg 13(8):634–636, 1982

55. Brinkley JR, Zappia RJ: An eyelid tumor caused by a migrated hard contact lens. Ophthalmic Surg 11(3):200–202, 1980

56. Friedberg ML, Abedi S: Encysted hard contact lens appearing as an orbital mass. Ophthal Plast Reconstr Surg 5(4):291–293, 1989

57. Roberts-Harry TJ, Cavey CC, Jagger JD: Periocular migration of hard contact lenses. Br J Ophthalmol 76(2):95–97, 1992

58. Korb DR, Allansmith MR, Greiner JV, et al: Prevalence of conjunctival changes in wearers of hard contact lenses. Am J Ophthalmol 90:336–341, 1980

59. Greiner JV, Allansmith MR: Effect of contact lens wear on the conjunctival mucous system. Ophthalmology 88:821–832, 1981

60. Gilbard JP, Gray KL, Rossi SR: A proposed mechanism for increased tear-film osmolarity in contact lens wearers. Am J Ophthalmol 102:505–507, 1986

61. Farris RL: The dry eye: Its mechanisms and therapy, with evidence that contact lens is a cause. CLAO J 12(4):234–246, 1986

62. Reitschel RL, Wilson LA: Ocular inflammation in patients using soft contact lenses. Arch Dermatol 118:147–149, 1982

63. Allansmith MR, Ross RN: Giant papillary conjunctivitis. Int Ophthalmol Clin 28(4):309–316, 1988

64. Donshik PC: Giant papillary conjunctivitis. Trans Am Ophthalmol Soc 92:687–744, 1994

65. Douglas JP, Lowder CY, Lazorik R, Meisler DM: Giant papillary conjunctivitis associated with rigid gas-permeable contact lenses. CLAO J 14(3):143–147, 1988

66. Begley CG, Riggle A, Tuel JA: Association of giant papillary conjunctivitis with seasonal allergies. Optom Vis Sci 67(3):192–195, 1990

67. Allansmith MR, Baird RS: Percentage of degranulated mast cells in vernal conjunctivitis and giant papillary conjunctivitis associated with contact-lens wear. Am J Ophthalmol 91:71–75, 1981

68. Barishak Y, Zavaro A, Samra Z, Sompolinsky D: An immunological study of papillary conjunctivitis due to contact lenses. Curr Eye Res 3(10):1161–1168, 1984

69. Goen TM, Sieboldt K, Terry JE: Cromolyn sodium in ocular allergic diseases. J Am Optom Assoc 57(7):526–529, 1986

70. Kruger CJ, Ehlers WH, Luistro AE, Donshik PC: Treatment of giant papillary conjunctivitis with cromolyn sodium. CLAO J 18(1):46–48, 1992

71. Wood TS, Stewart RH, Bowman RW, et al: Suprofen treatment of contact lens-associated giant papillary conjunctivitis. Ophthalmology 95:822–826, 1988

72. Bucci FA, Lopatynsky MO, Jenkins PL, et al: Comparison of the clinical performance of the Acuvue disposable contact lens and the CSI lens in patients with giant papillary conjunctivitis. Am J Ophthalmol 115:454–459, 1993

73. Porazinski AD, Donshik PC: Giant papillary conjunctivitis in frequent replacement contact lens wearers: A retrospective study. CLAO J 25(3):142–147, 1999

74. Sendele DD, Kenyon KR, Mobilia EF, et al: Superior limbic keratoconjunctivitis in contact lens wearers. Ophthalmology 90:616–622, 1983

75. Fuerst DJ, Sugar J, Worobec S: Superior limbic keratoconjunctivitis associated with cosmetic soft contact lens wear. Arch Ophthalmol 101:1214–1216, 1983

76. Hamburger HA: Pyogenic granuloma associated with extended wear contact lenses. CLAO J 12(2):99–100, 1986

77. Horton JC, Mathers WD, Zimmerman LE: Pyogenic granuloma of the palpebral conjunctiva associated with contact lens wear. Cornea 9(4):359–361, 1990

78. Ichijima H, Petroll WM, Jester JV, et al: Effects of increasing dk with rigid contact lens extended wear on rabbit corneal epithelium using confocal microscopy. Cornea 11(4):282–287, 1992

79. Lemp MA, Gold JB: The effects of extended-wear hydrophilic contact lenses on the corneal epithelium. Am J Ophthalmol 101:274–277, 1986

80. Tripathi BJ, Tripathi RC: Hydrogen peroxide damage to human corneal epithelial cells in vitro: Implications for contact lens disinfection systems. Arch Ophthalmol 107:1516–1519, 1989

81. Clinch TE, Goins KM, Cobo LM: Treatment of contact lens-related ocular surface disorder with autologous conjunctival transplantation. Ophthalmology 99:634–638, 1992

82. Guex-Crosier Y, Herbot CP: Presumed corneal intraepithelial neoplasia associated with contact lens wear and intense ultraviolet light exposure. Br J Ophthalmol 77:191–192, 1993

83. Bergmanson JPG, Chu LWF: Contact lens-induced corneal epithelial injury. Am J Optom Physiol Opt 59(6):500–506, 1982

84. Bloomfield SE, Jakobiec FA, Theodore FH: Contact lens induced keratopathy: A severe complication extending the spectrum of keratoconjunctivitis in contact lens wearers. Ophthalmology 91:290–294, 1984

85. Lohman LE: Corneal epithelial response to contact lens wear. CLAOJ 12(3):153–156, 1986

86. Udell IJ, Mannis MJ, Meisler DM, Langston RHS: Pseudodendrites in soft contact lens wearers. CLAO J 11(1):51–53, 1985

87. Margulies LJ, Mannis MJ: Dendritic corneal lesions associated with soft contact lens wear. Arch Ophthalmol 101:1551–1553, 1983

88. Seedor JA, Waring GO: Dendriform lesions of the cornea induced by soft contact lenses. Arch Ophthalmol 105:1021, 1987

89. Stainer GA, Brightbill FS, Holm P, Laux D: The development of pseudopterygia in hard contact lens wearers. Contact and Intraocul Lens Med J 7(1):1–4, 1981

90. Hayasaka S, Morihiro K, Shibasaki H, et al: Superficial punctate keratopathy and bacterial growth in patients with unilateral aphakia using extended-wear soft contact lenses. Ophthalmologica 204:169–174, 1992

91. Rosenfeld SI, Mandelbaum S, Corrent GF, et al: Granular epithelial keratopathy as an unusual manifestation of pseudomonas keratitis associated with extended-wear soft contact lenses. Am J Ophthalmol 109:17–22, 1990

92. Lindquist TD, Sher NA, Doughman DJ: Clinical signs and medical therapy of early acanthamoeba keratitis. Arch Ophthalmol 106:73–77, 1988

93. Madigan MC, Holden BA, Kwok LS: Extended wear of contact lenses can compromise corneal epithelial adhesion. Curr Eye Res 6(10):1257–1260, 1987

94. McMonnies CW: Contact lens intolerance in association with epithelial dystrophy. Am J Optom Physiol Opt 58(5):414–418, 1981

95. Udell IJ, Ormerod LD, Boniuk V, Abelson MB: Treatment of contact lens-associated corneal erosions (Letter). Am J Ophthalmol 104:306–307, 1987

96. Dangel ME, Kracher GP, Stark WJ: Anterior corneal mosaic in eyes with keratoconus wearing hard contact lenses. Arch Ophthalmol 102:888–890, 1984

97. Mobilia EF, Yamamoto GK, Dohlman CH: Corneal wrinkling induced by ultra-thin soft contact lenses. Ann Ophthalmol 103:371–375, 1980

98. Humphreys JA, Larke JR, Parrish ST: Microepithelial cysts observed inextended contact-lens wearing subjects. Br J Ophthalmol 64:888–889, 1980

99. Holden BA, Sweeney DF: The significance of the microcyst response: A review. Optom Vis Sci 68(9):703–707, 1991

100. Kenyon E, Polse KA, Seger RG: Influence of wearing schedule on extended-wear complications. Ophthalmology 93:231–236, 1986

101. Arentsen JJ: Corneal neovascularization in contact lens wearers. Int Ophthalmol Clin 26(1):15–23, 1986

102. Efron N: Vascular response of the cornea to contact lens wear. J Am Optom Assoc 58(10):836, 1987

103. McMonnies CW, Chapman-Davies A, Holden BA: The vascular response to contact lens wear. Am J Optom Physiol Opt 59(10):795–799, 1982

104. Duffin RM, Weissman BA, Glasser DB, Pettit TH: Flurbiprofen in the treatment of corneal neovascularization induced by contact lenses. Am J Ophthalmol 93:607–614, 1982 846, 1987

105. Lemp MA: The effect of extended-wear aphakic hydrophilic contact lenses after penetrating keratoplasty. Am J Ophthalmol 90:331–335, 1980

106. Bergenske PD, Polse KA: The effect of rigid gas permeable lenses on corneal sensitivity. J Am Optom Assoc 58(3):212–215, 1987

107. Beuerman RW, Rozsa AJ: Threshold and signal detection measurements of the effect of soft contact lenses on corneal sensitivity. Curr Eye Res 4(6):742–744, 1985

108. Rohde MD, Huff JW: Contact lens-induced edema in vitro-amelioration by lactate dehydrogenase inhibitors. Curr Eye Res 5(10):751–758, 1986

109. Bergmanson JPG, Chu LWF: Corneal response to rigid contact lens wear. Br J Ophthalmol 66:667–675, 1982

110. Johnson MH, Ruben CM, Perrigin DM: Entoptic phenomena and reproducibility of corneal striae following contact lens wear. Br J Ophthalmol 71:737–741, 1987

111. Lambert SR, Klyce SD: The origins of Sattler's veil. Am J Ophthalmol 91:51–56, 1981

112. Nirankari VS, Baer JC: Persistent corneal edema in aphakic eyes from daily-wear and extended-wear contact lenses. Am J Ophthalmol 98:329–335, 1984

113. Holden BA, Mertz GW: Critical oxygen levels to avoid corneal edema for daily and extended wear contact lenses. Invest Ophthalmol Vis Sci 25:1161–1167, 1984

114. O'Neal MR, Polse KA, Sarver MD: Corneal response to rigid and hydrogel lenses during eye closure. Invest Ophthalmol Vis Sci 25:837–842, 1984

115. Sarver MD, Polse KA, Baggett DA: Intersubject difference in corneal edema response to hypoxia. Am J Optom Physiol Opt 60(2):128–131, 1983

116. Holden BA, Mertz GW, McNally JJ: Corneal swelling response to contact lenses worn under extended wear conditions. Invest Ophthalmol Vis Sci 24:218–226, 1983

117. Sarver MD, Baggett DA, Harris MG, Louie K: Corneal edema with hydrogel lenses and eye closure: Effects of oxygen transmissibility. Am J Optom Physiol Opt 58(5):386–392, 1981

118. Nishida T, Yasumoto K, Morikawa Y, Otori T: Hard contact lens-induced corneal neovascularization treated by oxygenation. Cornea 10(4):358–360, 1991

119. Rozenman Y, Donnenfeld ED, Cohen EJ, et al: Contact lens-related deep stromal neovascularization. Am J Ophthalmol 107:27–32, 1989

120. Nirankari VS, Karesh J, Lakhanpal V, Richards RD: Deep stromal vascularization associated with cosmetic, daily-wear contact lenses. Arch Ophthalmol 101:46–47, 1983

121. Al-Hussaini AK, Friedlander MH, Karcioglu ZA: Intracorneal hemorrhage secondary to aphakic contact lens wear. Cornea 11(1):73–76, 1992

122. Donnenfeld ED, Ingraham H, Perry HD, et al: Contact lens-related deep stromal intracorneal hemorrhage. Ophthalmology 98:1793–1796, 1991

123. Yeoh RLS, Cox N, Falcon MG: Spontaneous intracorneal haemorrhage. Br J Ophthalmol 73:363–364, 1989

124. Braude LS, Sugar J: Circinate-pattern interstitial keratopathy in daily wear soft contact lens wearers. Arch Ophthalmol 103:1662–1665, 1985

125. Conway ST, Wagdi SF: Corneal scarring associated with daily soft contact lens wear. Ann Ophthalmol 15(9):868–871, 1983

126. Horowitz GS, Lin J, Chew HC: An unusual corneal complication of soft contact lens. Am J Ophthalmol 100:794–797, 1985

127. Chayet AS, Chayet J: An unusual corneal complication of soft contact lens (Letter). Am J Ophthalmol 101:623, 1986

128. Korb DR, Finnemore VM, Herman JP: Apical changes and scarring in keratoconus as related to contact lens fitting techniques. J Am Optom Assoc 53(3):199–205, 1982

129. Remeijer H, van Rij G, Beekhuis WH, et al: Deep corneal stromal opacities in long-term contact lens wear. Ophthalmology 97:281–285, 1990

130. Aquavella JV, DePaolis MD: Sterile infiltrates associated with contact lens wear. Int Ophthalmol Clin 31(2):121–126, 1991

131. Stein RM, Clinch TE, Cohen EJ, et al: Infected vs sterile corneal infiltrates in contact lens wearers. Am J Ophthalmol 105:632–636, 1988

132. Suchecki JK, Ehlers WH, Donshik PC: Peripheral corneal infiltrates associated with contact lens wear. CLAO J 22(1):41–46, 1996

133. Gordon A, Kracher GP: Corneal infiltrates and extended-wear contact lenses. J Am Optom Assoc 56(3):198–201, 1985

134. Bates AK, Morris RJ, Stapleton F, et al: Sterile corneal infiltrates in contact lens wearers. Eye 3:803–810, 1989

135. Crook T: Corneal infiltrates with red eye related to duration of extended wear. J Am Optom Assoc 56(9):698–700, 1985

136. Maguen E, Rosner I, Caroline P, et al: A retrospective study of disposable extended wear lenses in 100 patients: Year 2. CLAO J 18(4):229–231, 1992

137. Mondino BJ, Groden LR: Conjunctival hyperemia and corneal infiltrates with chemically disinfected soft contact lenses. Arch Ophthalmol 98:1167–1170, 1980

138. Stern GA: Corneal infections in contact lens wearers. Int Ophthalmol Clin 31(2):147–161, 1991

139. Poggio EC, Glynn RJ, Schein OD, et al: The incidence of ulcerative keratitis among users of daily-wear and extended-wear soft contact lenses. N Engl J Med 321:779–783, 1989

140. Schein OD, Glynn RJ, Poggio EC, et al: Microbial Keratitis Study Group: The relative risk of ulcerative keratitis among users of daily-wear and extended-wear soft contact lenses. N Engl J Med 321:773–778, 1989

141. Glynn RJ, Schein OD, Seddon JM, et al: The incidence of ulcerative keratitis among aphakic contact lens wearers in New England. Arch Ophthalmol 109:104–107, 1991

142. Galentine PG, Cohen EJ, Laibson PR, et al: Corneal ulcers associated with contact lens wear. Arch Ophthalmol 102:891–894, 1984 1986

143. Alfonso E, Mandelbaum S, Fox MJ, Forster RK: Ulcerative keratitis associated with contact lens wear. Am J Ophthalmol 101:429–433, 1986

144. Mondino BJ, Weissman BA, Farb MD, Pettit TH: Corneal ulcers associated with daily-wear and extended-wear contact lenses. Am J Ophthalmol 102:58–65, 1986

145. Ormerod LD, Smith RE: Contact lens-associated microbial keratitis. Arch Ophthalmol 104:79–83, 1986

146. Chalupa E, Swarbrick HA, Holden BA, Sjostrand J: Severe corneal infections associated with contact lens wear. Ophthalmology 94:17–22, 1987

147. Wilhelmus KR: Review of clinical experience with microbial keratitis associated with contact lenses. CLAO J 13(4):211–214, 1987

148. Derick RJ, Kelley CG, Gersman M: Contact lens related corneal ulcers at the Ohio State University Hospitals 1983–1987. CLAO J 15(4):268–270, 1989

149. Koidou-Tsiligianni A, Alfonso E, Forster RK: Ulcerative keratitis associated with contact lens wear. Am J Ophthalmol 108:64–67, 1989

150. Schein OD, Poggio EC: Ulcerative keratitis in contact lens wearers. Cornea 9(suppl 1):S55–S58, 1990

151. Cohen EJ, Gonzalez C, Leavitt KG, et al: Corneal ulcers associated with contact lenses including experience with disposable lenses. CLAO J 17(3):173–176, 1991

152. MacRae S, Herman C, Stulting D, et al: Corneal ulcer and adverse reaction rates in premarket contact lens studies. Am J Ophthalmol 111:457–465, 1991

153. Donnenfeld ED, Cohen EJ, Arentsen JJ, et al: Changing trends in contact lens associated corneal ulcers: An overview of 116 cases. CLAO J 12(3):145–149, 1986

154. Schein OD, Ormerod LD, Barraquer E, et al: Microbiology of contact lens-related keratitis. Cornea 8(4):281–285, 1989

155. Dart JKG: Predisposing factors in microbial keratitis: The significance of contact lens wear. Br J Ophthalmol 72:926–930, 1988

156. Musch DC, Sugar A, Meyer RF: Demographic and predisposing factors in corneal ulceration. Arch Ophthalmol 101:1545–1548, 1983

157. Rabinovitch J, Cohen EJ, Genvert GI, et al: Seasonal variation in contact lens-associated corneal ulcers. Can J Ophthalmol 22(3):155–156, 1987

158. Franks WA, Adams GGW, Dart JKG, Minassian D: Relative risks of different types of contact lenses. Br Med J 297:520–521, 1988

159. Aswad MI, John T, Barza M, et al: Bacterial adherence to extended wear soft contact lenses. Ophthalmol 97:296–302, 1990

160. Kent HD, Cohen EJ, Laibson PR, Arentsen JJ: Microbial keratitis and corneal ulceration associated with therapeutic soft contact lenses. CLAO J 16(1):49–52, 1990

161. Leibowitz HM: Clinical evaluation of ciprofloxacin 0.3% ophthalmic solution for treatment of bacterial keratitis. Am J Ophthalmol 112:34S–47S, 1991

162. Bowden FW, Cohen EJ, Arentsen JJ, Laibson PR: Patterns of lens care practices and lens product contamination in contact lens associated microbial keratitis. CLAO J 15(1):49–54, 1989

163. Wilson LA, Sawant AD, Simmons RB, Ahearn DG: Microbial contamination of contact lens storage cases and solutions. Am J Ophthalmol 110:193–198, 1990

164. Bilgin LK, Manav G, Tutkun IT, et al: Efficacy of a one-step hydrogen peroxide system for disinfection of soft contact lenses. CLAO J 19(1):50–52, 1993

165. Stern GA, Zam ZS: The effect of enzymatic contact lens cleaning on the adherence of pseudomonas aeruginosa to soft contact lenses. Ophthalmology 95:115–119, 1987

166. Adams CP, Cohen EJ, Laibson PR, et al: Corneal ulcers in patients with cosmetic extended-wear contact lenses. Am J Ophthalmol 96:705–709, 1983

167. Cohen EJ Laibson PJ, Arentsen JJ, Clemons CS: Corneal ulcers associated with cosmetic extended wear soft contact lenses. Ophthalmology 94:109–114, 1987

168. Weissman BA, Mondino BJ, Pettit TH, Hofbauer JD: Corneal ulcers asociated with extended-wear soft contact lenses. Am J Ophthalmol 97:476–481, 1984

169. Eichenbaum JW, Feldstein M, Podos SM: Extended-wear aphakic soft contact lenses and corneal ulcers. Br J Ophthalmol 66:663–666, 1982

170. Lemp MA, Blackman HJ, Wilson LA, Leveille AS: Gram-negative corneal ulcers in elderly aphakic eyes with extended wear lenses. Ophthalmol 90:60–63, 1984

171. Klotz SA, Misra RP, Butrus SI: Contact lens wear enhances adherence of pseudomonas aeruginosa and binding of lectins to the cornea. Cornea 9(3):266–270, 1990

172. Boles SF, Refojo MF, Leong F: Attachment of pseudomonas to human-worn, disposable etafilcon A contact lenses. Cornea 11(1):47–52, 1992

173. Beuhler PO, Schein OD, Stamler JF, et al: The increased risk of ulcerative keratitis among disposable soft contact lens users. Arch Ophthalmol 110:1555–1558, 1992

174. Dunn JP, Mondino BJ, Weissman BA, et al: Corneal ulcers associated with disposable hydrogel contact lenses. Am J Ophthalmol 108:113–117, 1989

175. Wilhelmus KR, Robinson NM, Font RA, et al: Fungal keratitis in contact lens wearers. Am J Ophthalmol 106:708–714, 1988

176. Wilson LA, Ahearn DG: Association of fungi with extended-wear soft contact lenses. Am J Ophthalmol 101:434–436, 1986

177. Berger RO, Streeten BW: Fungal growth in aphakic soft contact lenses. Am J Ophthalmol 91:630–633, 1981

178. Churner R, Cunningham RD: Fungal-contaminated soft contact lenses. Ann Ophthalmol 15(8):724–727, 1983

179. Moore MB, McCulley JP, Luckenbach M, et al: Acanthamoeba keratitis associated with soft contact lenses. Am J Ophthalmol 100:396–403, 1985

180. Stehr-Green JK, Bailey TM, Brandt FH, et al: Acanthamoeba keratitis in soft contact lens wearers: A case-control study. J Am Med Assoc 258:57–60, 1987

181. Moore MB, McCulley JP, Newton C, et al: Acanthamoeba keratitis: A growing problem in soft and hard contact lens wearers. Ophthalmology 94:1654–1661, 1987

182. Koenig SB, Solomon JM, Hyndiuk RA, et al: Acanthamoeba keratitis associated with gas-permeable contact lens wear (Letter). Am J Ophthalmol 103:832, 1988

183. Heidemann DG, Verdier DD, Dunn SP, Stamler JF: Acanthamoeba keratitis associated with disposable contact lenses. Am J Ophthalmol 110:630–634, 1990

184. Doren GS, Cohen EJ, Higgins SE, et al: Management of contact lens associated acanthamoeba keratitis. CLAO J 17(2):120–125, 1991

185. Penley CA, Willis SW, Sickler SG: Comparative antimicrobial efficacy of soft and rigid gas permeable contact lens solutions against acanthamoeba. CLAO J 15(4):257–260, 1989

186. Silvany RE, Dougherty JM, McCulley JP, et al: The effect of currently available contact lens disinfection systems on acanthamoeba castellanii and acanthamoeba polyphaga. Ophthalmology 97:286–290, 1990

187. Silvany RE, Dougherty JM, McCulley JP: Effect of contact lens preservatives on acanthamoeba. Ophthalmology 98:854–857, 1991

188. Ruiz-Montenegro J, Mafra CH, Wilson SE, et al: Corneal topographic alterations in normal contact lens wearers. Ophthalmol 100:128–134, 1993

189. Mobilia EF, Kenyon KR: Contact lens-induced corneal warpage. Int Ophthalmol Clin 26(1):43–53, 1986

190. Asbell PA, Wasserman D: Contact lens-induced corneal warpage. Int Ophthalmol Clin 31(2):121–126, 1991

191. Wilson SE, Lin DTC, Klyce SD, et al: Rigid contact lens decentration: A risk factor for corneal warpage. CLAO J 16(3):177–182, 1990

192. Phillips CI: Contact lenses and corneal deformation: Cause, correlate or coincidence? Acta Ophthalmol 68:661–668, 1990

193. Wilson SE, Lin DTC, Klyce SD, et al: Topographic changes in contact lens-induced corneal warpage. Ophthalmol 97:734–744, 1990

194. Krachmer JH, Feder RS, Belin MW: Keratoconus and related noninflammatory corneal thinning disorders. Surv Ophthalmol 28:293–322, 1984

195. Nauheim JS, Perry HD: A clinicopathologic study of contact lens-related keratoconus. Am J Ophthalmol 100:543–546, 1985

196. Macsai MS, Varley GA, Krachmer JH: Development of keratoconus after contact lens wear: Patient characteristics. Arch Ophthalmol 108:534–538, 1990

197. MacRae SM, Matsuda M, Shellans S: Corneal endothelial changes associated with contact lens wear. CLAO J 15(1):82–87, 1989

198. Holden BA, Williams L, Zantos SG: The etiology of transient endothelial changes in the human cornea. Invest Ophthalmol Vis Sci 26:1354–1359, 1985

199. Barr JT, Schoessler JP: Corneal endothelial response to rigid contact lenses. Am J Optom Physiol Opt 57(5):267–274, 1980

200. Holden BA, Williams L, Sweeney DF, Swarbrick HA: The endothelial response to contact lens wear. CLAO J 12(3):150–152, 1986

201. Stocker EG, Schoessler JP: Corneal endothelial polymegathism induced by PMMA contact lens wear. Invest Ophthalmol Vis Sci 26(6):857–863, 1985

202. Hirst LW, Auer C, Cohn J, et al: Specular microscopy of hard contact lens wearers. Ophthalmology 91:1147–1153, 1984

203. Yamauchi K, Hirst LW, Enger C, et al: Specular microscopy of hard contact lens wearers II. Ophthalmology 96:1176–1179, 1989

204. Orsborn GN, Schoessler JP: Corneal endothelial polymegathism after the extended wear of rigid gas-permeable contact lenses. Am J Optom Physiol Opt 65(2):84–90, 1988

205. Dada VK, Jain AK, Mehta MR: Specular microscopy of unilateral hard contact lens wearers. Indian J Ophthalmol 37(1):17–19, 1989

206. Matsuda M, Macrae SM, Inaba M, Manabe R: The effect of hard contact lens wear on the keratoconic corneal endothelium after penetrating keratoplasty. Am J Ophthalmol 107:246–251, 1989

207. Sibug ME, Datiles MB, Kashima K, et al: Specular microscopy studies on the corneal endothelium after cessation of contact lens wear. Cornea 10(5):395–401, 1991

208. MacRae SM, Matsuda M, Shellans S, Rich LF: The effects of hard and soft contact lenses on the corneal endothelium. Am J Ophthalmol 102:50–57, 1986

209. Lass JH, Dutt RM, Spurney RV, et al: Morphologic and fluorophotometric analysis of the corneal endothelium in long-term hard and soft contact lens wearers. CLAO J 14(2):105–109, 1988

210. Carlson KH, Bourne WM, Brubaker RF: Effect of long-term contact lens wear on corneal endothelial cell morphology and function. Invest Ophthalmol Vis Sci 29(2):185–193, 1988

211. Holden BA, Sweeney DF, Vannas A, et al: Effects of long-term extended contact lens wear on the human cornea. Invest Ophthalmol Vis Sci 26(11):1489–1501, 1985

212. Carlson KH, Bourne WM: Endothelial morphologic features and function after long-term extended wear of contact lenses. Arch Ophthalmol 106:1677–1679, 1988

213. Matsuda M, Inaba M, Suda T, Macrae SM: Corneal endothelial changes associated with aphakic extended contact lens wear. Arch Ophthalmol 106:70–72, 1988

214. Dutt RM, Stocker EG, Wolff CH, et al: A morphologic and fluorophotometric analysis of the corneal endothelium in long-term extended wear soft contact lens wearers. CLAO J 15(2):121–123, 1989

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