Giant papillary conjunctivitis is a common complication among soft contact lens wearers. This complication is often addressed by changing 1 of the following 3 factors:
1. Increasing the frequency of lens disposal
2. Decreasing the length of contact lens wear
3. Switching to a stronger cleaning solution
Rarely, rigid contact lenses can dislocate from the cornea and settle into the upper fornix. If undetected, the lens may erode through the conjunctiva and enter the soft tissues of the lid, where it can remain relatively asymptomatic. Alternatively, the tissues around the contact lens can become irritated and inflamed, producing a sterile abscess. The lens foreign body can incite the formulation of granulation tissue around the lens, encapsulating it in a cystlike structure.
A mechanical ptosis is occasionally the result of the mass of lens, scar, and fibrous tissue in the lid. An embedded contact lens also can produce enough scarring and contraction of the lid tissues to produce a lid retraction. The contact lens need not migrate into the lid tissues to produce ptosis. A ptotic lid can result simply from severe giant papillary conjunctivitis (GPC).
Occasionally, ptosis can be seen in contact lens wearers without any inflammation, lens migration, or other definite cause. Hard contact lens wearers may develop ptosis from levator aponeurosis disinsertion from years of repeated stretching of the lid during lens removal. A second proposed mechanism is that the repeated trauma of the lens edge rubbing against the palpebral conjunctiva produces chronic inflammation and edema in the soft tissues of the lid. Because all or part of the ptosis may resolve with discontinuation of contact lens wear, it is recommended that patients stop wearing their lenses for a period of time prior to surgical correction of the ptosis.
Tear Film
The tear film provides a smooth and transparent refractive surface, essential moisture, and oxygen to the epithelial cells. Tears also contain immunoglobulins, complement, and other proteins, which help protect against infection. The health of the ocular surface is entirely dependent upon an adequate quantity and quality of tear film, both of which can be altered by the presence of contact lenses.
Bacteria and debris are collected in the tear film, wiped by the lid blink, and rinsed away from the surface of the eye. The presence of a contact lens on the eye substantially reduces the interchange of tears across the ocular surface. Rigid lenses reduce the tear exchange compared to no contact lens wear. Soft lenses reduce the tear exchange to an even greater extent and the larger the diameter, the greater the reduction.
The effect of contact lenses on the tear film can vary from one part of the cornea to another part of the cornea. Tear film instability exists in the interpalpebral fissure in the periphery of the cornea, the so-called 3- and 9-o'clock areas, in wearers of rigid contact lenses. A rigid lens that is fit poorly often produces corneal staining at these sites. Epithelial damage in these areas is associated with instability and abnormalities in the mucin layer of the tear film.
In addition to the mixing of tears, the content of the tears can be altered by the presence of contact lenses. Overnight wear increases the levels of tear proteins compared to daily wear or no wear of contact lenses.
The tear film provides a smooth and transparent refractive surface, essential moisture, and oxygen to the epithelial cells. Tears also contain immunoglobulins, complement, and other proteins, which help protect against infection. The health of the ocular surface is entirely dependent upon an adequate quantity and quality of tear film, both of which can be altered by the presence of contact lenses.
Bacteria and debris are collected in the tear film, wiped by the lid blink, and rinsed away from the surface of the eye. The presence of a contact lens on the eye substantially reduces the interchange of tears across the ocular surface. Rigid lenses reduce the tear exchange compared to no contact lens wear. Soft lenses reduce the tear exchange to an even greater extent and the larger the diameter, the greater the reduction.
The effect of contact lenses on the tear film can vary from one part of the cornea to another part of the cornea. Tear film instability exists in the interpalpebral fissure in the periphery of the cornea, the so-called 3- and 9-o'clock areas, in wearers of rigid contact lenses. A rigid lens that is fit poorly often produces corneal staining at these sites. Epithelial damage in these areas is associated with instability and abnormalities in the mucin layer of the tear film.
In addition to the mixing of tears, the content of the tears can be altered by the presence of contact lenses. Overnight wear increases the levels of tear proteins compared to daily wear or no wear of contact lenses.
Conjunctiva
Conjunctival Abnormalities
Contact allergy
A contact dermatitis hypersensitivity reaction can be produced by one of a host of chemicals, which are found in contact lens solutions. A typical reaction consists of marked itching with varying amounts of injection, burning, redness, tearing, mucoid discharge, and occasionally chemosis. In addition, the lid may become edematous and erythematous. Cold compresses and the elimination of the offending chemical usually relieves symptoms. A short course of topical steroids can be used in particularly severe instances.
Giant papillary conjunctivitis
Approximately 1-3% of contact lens wearers eventually develop a symptom complex of GPC consisting of conjunctival injection, mucoid discharge, itching, tear film debris, coated lenses, blurred vision, excess lens movement, and blurred vision. These symptoms may remain minimal or progress to complete lens intolerance. The tarsal conjunctiva becomes inflamed and hypertrophied. This inflammatory hypertrophy is morphologically similar to the papillary hypertrophy of vernal conjunctivitis.
The etiology of GPC is multifactorial and begins with the formation of deposits on the surface of the lens. The constant trauma of the blinking lid rubbing on the surface of the lens exposes the deposits to the conjunctival lymphatic system. The antigens associated with the deposits incite an immune response in the conjunctiva. This condition can occur whenever a foreign substance chronically rubs the tarsal conjunctiva, such as ocular prostheses, exposed scleral buckles, nylon sutures, and gas-permeable contact lenses but most commonly is associated with soft contact lenses.
Typically, papillae (0.3 mm or larger) are seen surrounded by thickened and hypervascular conjunctiva. The hyperplastic epithelium extends down into the underlying stoma. The epithelium is infiltrated with mast cells, and the stroma is infiltrated with basophils and eosinophils. The symptoms of GPC are exacerbated by anything that increases the contact of the lens deposits with the tarsal conjunctiva, such as increased numbers of deposits, increased size of the contact lens, and increased wearing time, especially overnight wear.
Treatment of GPC consists of reducing the amount of contact between the deposits and the conjunctiva. Frequent enzymatic cleaning of the contact lenses, frequent replacement of contact lenses (disposable lenses), reduction in wearing time, and the use of lenses that resist deposit formation are effective treatments.
Medications that suppress the immune response also can be used. Topical steroids also reduce symptoms; however, the risk of complications limits their use. Topical mast cell stabilizers, such as 4% cromolyn, have some effectiveness in reducing the symptoms of GPC. Medical treatments generally are used for a short duration in acute exacerbations. The most effective treatment usually is reduced wearing time and switching to disposable contact lenses.
Contact lens–induced superior limbic keratoconjunctivitis
Contact lens–induced superior limbic keratoconjunctivitis (CL-SLK) is an immunologic reaction in the peripheral conjunctiva produced by contact lens wear that is similar to that seen in Theodore superior limbic keratoconjunctivitis (SLK). It is characterized by conjunctival thickening, erythema, and a variable amount of fluorescein staining of the superior bulbar conjunctiva.
The keratinized epithelium loses many of its goblet cells and is invaded by neutrophils. Foreign body sensation, photophobia, tearing, burning, occasional itching, and reduced visual acuity due to punctate epitheliopathy are typical symptoms of CL-SLK.
Although similar in name, CL-SLK is a separate and distinct entity from Theodore SLK. CL-SLK can be differentiated by a lack of filaments, minimal tarsal papillary reaction, impaired vision, and lack of association with thyroid disease. It also is not limited to the superior conjunctiva but can be circumferential.
CL-SLK may be caused by excessive lens movement or sensitivity to thimerosal. Treatment consists of discontinuing contact lens wear until the epithelium returns to normal and the symptoms resolve. Refitting with better fitting lenses, using preservative-free solutions with a hydrogen peroxide disinfecting system, or switching to rigid gas-permeable (RGP) contact lenses may permit a resumption of contact lens wear.
Corneal Epithelium
Mechanical epithelial defects
The contact lens is a foreign body that rubs across and is pressed against the corneal epithelium with each blink, thousands of times each day. Surprisingly, this only occasionally results in an abrasion. Corneal abrasions from contact lens wear need to be recognized and treated because they indicate chronic epithelial stress due to the contact lens. Epithelial defects can allow bacteria to penetrate the cornea, resulting in a stromal infection. Chronic corneal epithelial trauma can stimulate subepithelial fibrosis in the absence of an infection. The specific abrasion pattern often provides the necessary clues to indicate what problem can be corrected to improve the comfort and safety of the patient.
Manipulation of a contact lens during insertion and removal can traumatize the epithelium creating painful abrasions of various shapes and sizes. These abrasions usually heal quite rapidly with simple lubrication or patching. Debris trapped under a contact lens or a chip or tear in the edge of a contact lens can produce dramatic curvilinear abrasions. Removal of the debris or replacement of the damaged contact lens is all that is needed to treat this problem.
Punctate epithelial erosions occur commonly with contact lens wear and have several causes. Three staining patterns are characteristic for rigid lenses, as follows: central, peripheral, and 3- and 9-o'clock positions. If a lens is too flat for the particular cornea, it may produce central punctate staining. A steep cornea, such as in keratoconus where the lens rubs on the tip of the cone, is a typical example. A lens that is too steep for the cornea can produce peripheral punctate staining patterns, often in a superior arcuate shape. A poorly moving lens or one with a large optical zone may produce superior arcuate staining.
The most common staining pattern occurs between the lens and the limbus in the interpalpebral fissure (at the 3- and 9-o'clock positions). This epitheliopathy is caused by the contact lens lifting the lid away from the cornea and poor tear stability with subsequent drying of the cornea. This often is exacerbated by an incomplete blink. A small amount of staining (at the 3- and 9-o'clock positions) is benign, but persistent epithelial erosions can lead to dellen formation, neovascularization, Salzmann-type elevated lesions, and pseudopterygium formation. This type of punctate staining is alleviated by decreasing the distance from the lens to the limbus with a larger lens, reducing edge lift with a thinner-edged lens or steeper fit, or refitting with a lens that rests under the upper lid (alignment fit).
Punctate staining by soft lenses is not as common as with rigid lenses but can occur. Soft lenses that cause excessive desiccation can cause an inferior central or inferior arcuate pattern. Usually, these patients have minor symptoms of mild irritation or slightly decreased vision. Refitting with a higher water content lens or RGP lens usually eliminates the problem.
Epithelial splitting is a common finding in asymptomatic soft contact lens wearers. This finding often is overlooked on a routine examination because it usually does not cause severe symptoms and may be covered by the upper lid. Epithelial splits are horizontal, linear, white, faintly staining epithelial defects in the superior cornea, which often are asymptomatic during lens wear and produce mild foreign body sensation after the lens has been removed. The splits usually heal after the lenses have been out for 24 hours and refitting with RGP lenses prevents recurrence.
Chemical epithelial defects
Various contact lens chemical solutions can produce a range of epithelial defects from marked erosions to less extensive punctate defects. Surfactant cleaning solutions that are left on the lens after cleaning usually cause immediate pain, redness, photophobia, and tearing upon lens insertion. These symptoms typically disappear after 1-2 days.
If hydrogen peroxide is placed on the eye, it can cause intraepithelial and subepithelial gas bubbles. These bubbles have a dramatic appearance and can cause significant but usually temporary vision loss. The bubbles typically resolve without permanent sequelae within minutes to hours. However, hydrogen peroxide can cause a permanent refractive change by altering the shape of the cornea.
Enzyme cleaner and chemical disinfection solutions can cause more subtle and intermittent punctate epithelial defects. This condition may require careful investigation and systematic elimination of various lens care products to identify and remove the offending agent. Use of preservative-free solutions and proper use of hydrogen peroxide disinfection usually solves this problem.
Hypoxia
Because the oxygen requirements of the cornea are met by direct diffusion of oxygen from the corneal surface, the barrier of the contact lens reduces the amount of available oxygen. Contact lens wear (especially with a closed lid during sleep) can cause acute hypoxia. If mild, hypoxia produces epithelial edema and temporary blurred vision; if severe, it can cause epithelial cell death and desquamation. Patients usually experience discomfort and remove the contact lenses before the acute hypoxia becomes severe. Typically, the conjunctiva is hyperemic, and the epithelium has fine punctate defects, producing temporary decreased vision and photophobia.
Chronic hypoxia produces a variety of more subtle effects, such as epithelial microcysts. Contact lens users who sleep in their lenses are prone to developing epithelial microcysts. These transparent epithelial inclusions of degenerated epithelium are about 10-15 ﾵm, begin in the deep epithelium, and slowly migrate anteriorly. Upon reaching the surface, they rupture, creating depressions that pool with fluorescein. Epithelial microcysts seldom produce any significant symptoms other than a mild decrease in vision. Surprisingly, it takes several weeks for the microcysts to disappear after discontinuation of the contact lenses. Either the mitotic rate is reduced below normal or the microcysts continue to be produced long after the contact lenses are removed.
One of the hallmarks of chronic corneal hypoxia is superficial neovascularization, especially along the superior limbus. Neovascularization of less than 2 mm from the limbus is not visually significant and generally is well tolerated but is a sign of hypoxia and may be a harbinger of more significant problems. Rarely, deep stromal neovascularization can occur. Changing to lenses that are thinner or contain materials with greater oxygen permeability, have greater lens movement, and decreasing wear time (especially eliminating overnight wear) can greatly reduce the risk of progression. Chronic hypoxia has been implicated as a cause of the decreased corneal sensitivity that occurs with prolonged contact lens wear and may be partly the reason why some patients have increased comfort with long-term wear and why they often have decreased comfort with a change from polymethyl methacrylate (PMMA) to gas-permeable contact lenses.
The corneal epithelium is thinner in contact lens wearers. This change may be due to chronic hypoxia and decreased mitotic activity. In addition to thinning of the epithelium, extended wear is associated with decreased epithelial shedding, increased cell size, and increased binding of Pseudomonas aeruginosa to the cell surface. All of these effects could reduce the resistance of the cornea to bacterial infection. The thinner epithelium poses less of a barrier to bacterial penetration. The reduced shedding of epithelial cells allows the attached bacteria to remain on the eye for longer periods of time. The increased binding of bacteria, such as P aeruginosa, enables greater numbers of bacteria to attach to the epithelial surface.
The physiology of the corneal epithelium also is altered by contact lens wear. The barrier function of the epithelium is reduced, and the permeability to fluorescein is doubled after as little as 2 weeks of soft contact lens wear. Similarly, rigid contact lenses can alter the epithelial permeability.
Superficial immunologic reactions
A variety of chemicals in contact lens solutions can elicit superficial toxic or immune reactions. The typical response is a fine punctate keratopathy, conjunctival injection, tearing, itching, and occasionally chemosis.
The preservative, thimerosal, which is now rarely used, produced a keratoconjunctivitis in as many as 10% of contact lens wearers who used thimerosal-preserved products. Essentially, it has disappeared from use, but other chemicals used as preservatives or disinfectives can produce similar pathology, so recognition of this condition is helpful.
The earliest symptoms are mild and nonspecific (eg, foreign body sensation, conjunctival hyperemia, variable mixed follicular-papillary hypertrophy), which present gradually after weeks or years of uneventful contact lens wear. The superior limbus becomes progressively more hyperemic and a triangle of punctate keratopathy extends downward from the involved limbus toward the central cornea. If allowed to proceed, the epitheliopathy may progress to an opaque pannus with microcysts.
A problem associated with the use of chemical disinfection systems and seen with increasing frequency is the development of small, gray, epithelial, granular opacities that resemble the epithelial opacities of Thygeson superficial punctate keratopathy. The round, gray-white granules appear to be on the surface of the epithelium and are scattered randomly across the cornea. They are similar to Thygeson superficial punctate keratopathy, but they tend to be small and stain less intensely with fluorescein. These opacities are associated with symptoms of foreign body sensation, tearing, photophobia, lens intolerance, and conjunctival injection. The symptoms resolve over a few days after the chemical disinfecting solution is discontinued.
Thimerosal and other chemicals used in disinfection systems also can produce subepithelial infiltrates similar to those seen in adenoviral conjunctivitis. Changing to a preservative-free hydrogen peroxide based disinfection system or to gas-permeable lenses allows these deposits and infiltrates to resolve. However, it may take weeks for the pathology to disappear.
Corneal Stroma
Sterile infiltrates
Contact lens wear can induce a distinctive sterile keratitis, which presents as a sudden onset of an anterior stromal or subepithelial polymorphonuclear leukocyte and mononuclear cell infiltrate typically in the periphery of the cornea. The infiltrates usually are small (0.1-2 mm) and may be single or in groups. The infiltrates may be round, oval, or arcuate and may underlie either an intact epithelium or an epithelial defect.
Histologic examination of biopsy specimens of these infiltrates reveals focal areas of full-thickness loss of epithelium with surrounding thin areas of epithelium. The polymorphonuclear leukocyte infiltrates were localized directly under the Bowman layer, and patchy areas of necrosis were present. The specimens did not reveal any microorganisms.
The etiology of these sterile infiltrates may involve an immune-mediated reaction to bacterial toxins from colonized contact lenses. Staphylococcal organisms have been isolated from contact lens wearers that have sterile infiltrates. The infiltrates tend to resolve with no loss of vision leaving behind only a faint scar in the anterior stroma after a short course of topical steroids or simple elimination of contact lens wear.
Usually, sterile infiltrates can be differentiated from infectious infiltrates on clinical signs and symptoms alone. Sterile infiltrates tend to be multiple, peripheral, associated with less pain, minimal anterior chamber inflammation, and with less of an epithelial defect than infectious ulcers. However, if doubt exists, they should be treated as presumed infectious ulcers.
Infectious keratitis
Microbial keratitis is an uncommon but potentially devastating complication of contact lens wear.2 The eye is under constant threat of infection, primarily by bacteria present on the lids and in the tears. Fortunately, the eye has many defense mechanisms with which to fend off the bacterial invaders.
The lids constantly wipe the ocular surface, mechanically dislodging bacteria and epithelial cells from the surface. The constant flow of tears across the eye continually washes away bacteria and debris from the eye and into the nasolacrimal ducts. The tears not only have a dilutional effect but also contain immunoglobulins, lysozyme, and compliment, which can inactivate potential pathogens.
The multiple layers of epithelial cells provide a formidable barrier to bacterial infection. The mucin-coated surface is resistant to bacterial adhesion. The constant shedding of desquamating epithelial cells rid the eye of attached bacteria. The multiple layers of epithelial cells give the ocular surface extra security. If one layer of cells is penetrated, it can be sloughed, while the remaining layers remain to provide continued protection.
The cornea is richly innervated with sensory nerves, which respond to bacterial toxins, inflammation, and epithelial defects. The resultant pain increases tearing and blinking resulting in increased protection.
All of these protective mechanisms are affected adversely by contact lens wear. The contact lens is a barrier between the epithelial surface and the lid preventing the wiping action of the lid. Tear exchange is reduced markedly under the contact lens, creating a stagnant pool of tears next to the cornea.
Contact lens wear reduces the thickness of the epithelium, reduces the rate of cell turnover and desquamation, and increases the ability of bacteria to adhere to epithelial cells. With the reduced corneal sensitivity associated with contact lens wear, the early stages of infection may not be felt as much; thus, the reflex tearing and blinking responses may be blunted.
Contact lenses also cause breaks in the epithelium (eg, punctate erosions, abrasions, splits), which allow direct access of pathogens to the stroma. The epithelium of the contact lens wearer is thinner, less sensitive, and relatively hypoxic; all of these factors reduce the ability of the epithelium to repair itself and repel invading organisms.
In the United States, one in 2,500 daily contact lens wearers and 1 in 500 overnight wearers develop bacterial keratitis each year. A variety of both gram-positive organisms and gram-negative organisms have been isolated from corneal infections. However, the most commonly cultured pathogens have been P aeruginosa, Staphylococcus aureus, and Staphylococcus epidermidis. This trend may be changing in the direction of increased frequency of gram-positive organisms. The high association of P aeruginosa may be because of its ability to invade corneal epithelial cells.
Case reports of contact lens-associated corneal infections first appeared in the ophthalmic literature 2 decades ago. Contact lenses were implicated as a causative factor, but it was not until the hallmark studies of Schein and colleagues that the incidence and relative risk of contact lens-associated corneal infections was elucidated. They found the incidence of ulcerative keratitis in New England to be 4.1 in 10,000 daily contact lens wearers per year. Incidence in extended contact lens wearers was even greater at 20.9 per 10,000. When the actual wearing patterns of users were studied, they found that patients who slept in their lenses had a 10- to 15-fold higher risk of developing an infection. Incidence in the United Kingdom and the Netherlands is similar.
The introduction of disposable lenses did not reduce the risk of infection; in fact, the risk of infectious keratitis in disposable lens wearers was increased relative to daily wear soft or gas-permeable lenses. More recent studies also have found the risk of microbial keratitis to be increased with disposable contact lenses even when other risk factors were controlled. However, the primary risk factor for developing contact lens-related bacterial keratitis is sleeping with the lenses in. Similar to cosmetic contact lenses, aphakic extended wear increases the risk of infection.
Contact lens disinfecting solutions themselves can also contribute to infectious keratitis, as approximately one half of contact lens disinfecting solutions have been found to be contaminated with bacteria. Contact lens care solutions were also implicated in a recent outbreak of Fusarium keratitis in Asia and in the United States.3
Breaks in the corneal epithelium probably are important predisposing factors to bacterial keratitis. However, they are not a necessary precondition. P aeruginosa can penetrate intact epithelium, and bacterial keratitis can occur on the surface of the intact epithelium.
The symptoms of bacterial keratitis usually present acutely (within 24 h) and include pain, photophobia, tearing, purulent discharge, and reduced vision. Early in the course of the disease a whitish-to-yellow stromal infiltrate develops under an epithelial defect in the presence of anterior chamber reaction and conjunctival injection. This progresses to stromal and epithelial edema, anterior chamber reaction, hypopyon, and eventually stromal necrosis. Often, gram-negative bacteria induce an immune precipitate (Wessely ring) to form around the nidus of infection. The firm diagnosis of bacterial infection is made with a positive culture; however, even with the best culture techniques, cultures often are negative and treatment must be empirical. The mainstay of treatment has consisted of broad-spectrum topical antibiotics (eg, combination of cefazolin 50 mg/mL and tobramycin 14 mg/mL) administered at frequent intervals, starting at every 15-30 minutes, and less frequent as the clinical response allows. These doses of antibiotics are quite toxic and need to be tapered to prevent epithelial damage.
Ciprofloxacin 0.3% and ofloxacin 0.3% may be as effective in treating bacterial keratitis as the traditional combination of fortified antibiotics and are commercially available. However, with the ever-changing spectrum of microbial resistance, it is recommended to culture every serious keratitis and treat according to the antibiotic sensitivities. Fortunately, with prompt antibiotic therapy, most bacterial corneal infections can be cured with little sequelae.
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47. Krachmer JH, Purcell JJ Jr. Bacterial corneal ulcers in cosmetic soft contact lens wearers. Arch Ophthalmol. Jan 1978;96(1):57-61. [Medline].
48. 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. Apr-Jun 1988;14(2):105-9. [Medline].
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50. Levenson JE. Corneal damage from improperly cleaned tonometer tips. Arch Ophthalmol. Aug 1989;107(8):1117. [Medline].
51. Levine ML, Serdarevic ON. Increasing fluoroquinolone resistance and predominance of gram-positive organisms in contact lens-related corneal ulcers. Ophthalmology. 1996;103:145.
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53. Liu Z, Pflugfelder SC. The effects of long-term contact lens wear on corneal thickness, curvature, and surface regularity. Ophthalmology. Jan 2000;107(1):105-11. [Medline].
54. Mac Rae SM, Matsuda M, Shellans S, Rich LF. The effects of hard and soft contact lenses on the corneal endothelium. Am J Ophthalmol. Jul 15 1986;102(1):50-7. [Medline].
55. MacRae SM, Matsuda M, Phillips DS. The long-term effects of polymethylmethacrylate contact lens wear on the corneal endothelium. Ophthalmology. Feb 1994;101(2):365-70. [Medline].
56. Malinovsky V, et al. Epithelial splits of the superior cornea in hydrogel contact lens patients. ICLC. 1989;16:252-4.
57. Matthews TD, Frazer DG, Minassian DC, et al. Risks of keratitis and patterns of use with disposable contact lenses. Arch Ophthalmol. Nov 1992;110(11):1559-62. [Medline].
58. McLeod SD, Goei SL, Taglia DP, McMahon TT. Nonulcerating bacterial keratitis associated with soft and rigid contact lens wear. Ophthalmology. Mar 1998;105(3):517-21. [Medline].
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61. Miller RA, Brightbill FS, Slama SL. Superior limbic keratoconjunctivitis in soft contact lens wearers. Cornea. 1982;1:293.
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67. Nieuwendaal CP, Odenthal MT, Kok JH, et al. Morphology and function of the corneal endothelium after long-term contact lens wear. Invest Ophthalmol Vis Sci. Jun 1994;35(7):3071-7. [Medline].
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69. O'Brien TP, Maguire MG, Fink NE, Alfonso E, McDonnell P. Efficacy of ofloxacin vs cefazolin and tobramycin in the therapy for bacterial keratitis. Report from the Bacterial Keratitis Study Research Group. Arch Ophthalmol. Oct 1995;113(10):1257-65. [Medline].
70. Orsborn GN, Zantos SG. Corneal desiccation staining with thin high water content contact lenses. CLAO J. Apr-Jun 1988;14(2):81-5. [Medline].
71. 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. Sep 21 1989;321(12):779-83. [Medline].
72. Polse KA, Brand RJ, Cohen SR, Guillon M. Hypoxic effects on corneal morphology and function. Invest Ophthalmol Vis Sci. Aug 1990;31(8):1542-54. [Medline].
73. Radford CF, Minassian DC, Dart JK. Disposable contact lens use as a risk factor for microbial keratitis. Br J Ophthalmol. Nov 1998;82(11):1272-5. [Medline].
74. Ren DH, Petroll WM, Jester JV, et al. The effect of rigid gas permeable contact lens wear on proliferation of rabbit corneal and conjunctival epithelial cells. CLAO J. Jul 1999;25(3):136-41. [Medline].
75. Ren DH, Petroll WM, Jester JV, et al. The relationship between contact lens oxygen permeability and binding of Pseudomonas aeruginosa to human corneal epithelial cells after overnight and extended wear. CLAO J. Apr 1999;25(2):80-100. [Medline].
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93. Vallas V, Stapleton F, Willcox MD. Bacterial invasion of corneal epithelial cells. Aust N Z J Ophthalmol. Jun-Aug 1999;27(3-4):228-30. [Medline].
94. van den Bosch WA, Lemij HG. Blepharoptosis induced by prolonged hard contact lens wear. Ophthalmology. Dec 1992;99(12):1759-65. [Medline].
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41. Itoh R, Yokoi N, Kinoshita S. Tear film instability induced by rigid contact lenses. Cornea. Jul 1999;18(4):440-3. [Medline].
42. Jalbert I, Stapleton F. Effect of lens wear on corneal stroma: preliminary findings. Aust N Z J Ophthalmol. Jun-Aug 1999;27(3-4):211-3. [Medline].
43. Jalbert I, Willcox MD, Sweeney DF. Isolation of Staphylococcus aureus from a contact lens at the time of a contact lens-induced peripheral ulcer: case report. Cornea. Jan 2000;19(1):116-20. [Medline].
44. Jupiter D, Karesh J. Ptosis associated with PMMA/rigid gas permeable contact lens wear. CLAO J. Jul 1999;25(3):159-62. [Medline].
45. Kok JH, Boets EP, van Best JA, Kijlstra A. Fluorophotometric assessment of tear turnover under rigid contact lenses. Cornea. Nov 1992;11(6):515-7. [Medline].
46. Kozer-Bilgin L, Demir N, Altan-Yaycioglu R. Microbiological evaluation of contact lenses and contact lens disinfection solutions in an asymptomatic population and in medical personnel. CLAO J. Oct 1999;25(4):228-32. [Medline].
47. Krachmer JH, Purcell JJ Jr. Bacterial corneal ulcers in cosmetic soft contact lens wearers. Arch Ophthalmol. Jan 1978;96(1):57-61. [Medline].
48. 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. Apr-Jun 1988;14(2):105-9. [Medline].
49. Levenson DS. Changes in corneal curvature with long-term PMMA contact lens wear. CLAO J. Apr-Jun 1983;9(2):121-5. [Medline].
50. Levenson JE. Corneal damage from improperly cleaned tonometer tips. Arch Ophthalmol. Aug 1989;107(8):1117. [Medline].
51. Levine ML, Serdarevic ON. Increasing fluoroquinolone resistance and predominance of gram-positive organisms in contact lens-related corneal ulcers. Ophthalmology. 1996;103:145.
52. Levy B, Stamper RL. Acute ptosis secondary to contact lens wear. Optom Vis Sci. Jul 1992;69(7):565-6. [Medline].
53. Liu Z, Pflugfelder SC. The effects of long-term contact lens wear on corneal thickness, curvature, and surface regularity. Ophthalmology. Jan 2000;107(1):105-11. [Medline].
54. Mac Rae SM, Matsuda M, Shellans S, Rich LF. The effects of hard and soft contact lenses on the corneal endothelium. Am J Ophthalmol. Jul 15 1986;102(1):50-7. [Medline].
55. MacRae SM, Matsuda M, Phillips DS. The long-term effects of polymethylmethacrylate contact lens wear on the corneal endothelium. Ophthalmology. Feb 1994;101(2):365-70. [Medline].
56. Malinovsky V, et al. Epithelial splits of the superior cornea in hydrogel contact lens patients. ICLC. 1989;16:252-4.
57. Matthews TD, Frazer DG, Minassian DC, et al. Risks of keratitis and patterns of use with disposable contact lenses. Arch Ophthalmol. Nov 1992;110(11):1559-62. [Medline].
58. McLeod SD, Goei SL, Taglia DP, McMahon TT. Nonulcerating bacterial keratitis associated with soft and rigid contact lens wear. Ophthalmology. Mar 1998;105(3):517-21. [Medline].
59. McNamara NA, Polse KA, Brand RJ, et al. Tear mixing under a soft contact lens: effects of lens diameter. Am J Ophthalmol. Jun 1999;127(6):659-65. [Medline].
60. McNamara NA, Polse KA, Fukunaga SA, et al. Soft lens extended wear affects epithelial barrier function. Ophthalmology. Dec 1998;105(12):2330-5. [Medline]. [Full Text].
61. Miller RA, Brightbill FS, Slama SL. Superior limbic keratoconjunctivitis in soft contact lens wearers. Cornea. 1982;1:293.
62. Millodot M, O'Leary DJ. Effect of oxygen deprivation on corneal sensitivity. Acta Ophthalmol (Copenh). Jun 1980;58(3):434-9. [Medline].
63. Mondino BJ, Groden LR. Conjunctival hyperemia and corneal infiltrates with chemically disinfected soft contact lenses. Arch Ophthalmol. Oct 1980;98(10):1767-70. [Medline].
64. Moore MB, McCulley JP, Kaufman HE, Robin JB. Radial keratoneuritis as a presenting sign in Acanthamoeba keratitis. Ophthalmology. Oct 1986;93(10):1310-5. [Medline].
65. Moore MB, McCulley JP, Luckenbach M, et al. Acanthamoeba keratitis associated with soft contact lenses. Am J Ophthalmol. Sep 15 1985;100(3):396-403. [Medline].
66. Nicolitz E, Flanagan JC. Orbital mass as a complication of contact lens wear. Arch Ophthalmol. Dec 1978;96(12):2238-9. [Medline].
67. Nieuwendaal CP, Odenthal MT, Kok JH, et al. Morphology and function of the corneal endothelium after long-term contact lens wear. Invest Ophthalmol Vis Sci. Jun 1994;35(7):3071-7. [Medline].
68. Nilsson SE, Lindh H. Daily contact lens wear. A three year follow-up. Acta Ophthalmol (Copenh). Aug 1984;62(4):556-65. [Medline].
69. O'Brien TP, Maguire MG, Fink NE, Alfonso E, McDonnell P. Efficacy of ofloxacin vs cefazolin and tobramycin in the therapy for bacterial keratitis. Report from the Bacterial Keratitis Study Research Group. Arch Ophthalmol. Oct 1995;113(10):1257-65. [Medline].
70. Orsborn GN, Zantos SG. Corneal desiccation staining with thin high water content contact lenses. CLAO J. Apr-Jun 1988;14(2):81-5. [Medline].
71. 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. Sep 21 1989;321(12):779-83. [Medline].
72. Polse KA, Brand RJ, Cohen SR, Guillon M. Hypoxic effects on corneal morphology and function. Invest Ophthalmol Vis Sci. Aug 1990;31(8):1542-54. [Medline].
73. Radford CF, Minassian DC, Dart JK. Disposable contact lens use as a risk factor for microbial keratitis. Br J Ophthalmol. Nov 1998;82(11):1272-5. [Medline].
74. Ren DH, Petroll WM, Jester JV, et al. The effect of rigid gas permeable contact lens wear on proliferation of rabbit corneal and conjunctival epithelial cells. CLAO J. Jul 1999;25(3):136-41. [Medline].
75. Ren DH, Petroll WM, Jester JV, et al. The relationship between contact lens oxygen permeability and binding of Pseudomonas aeruginosa to human corneal epithelial cells after overnight and extended wear. CLAO J. Apr 1999;25(2):80-100. [Medline].
76. Robin JB, Regis-Pacheco LF, May WN, et al. Giant papillary conjunctivitis associated with an extruded scleral buckle. Case report. Arch Ophthalmol. May 1987;105(5):619. [Medline].
77. 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. Jan 15 1990;109(1):17-22. [Medline].
78. Samples JR, Binder PS, Luibel FJ, et al. Acanthamoeba keratitis possibly acquired from a hot tub. Arch Ophthalmol. May 1984;102(5):707-10. [Medline].
79. Sanaty M, Temel A. Corneal sensitivity changes in long-term wearing of hard polymethylmethacrylate contact lenses. Ophthalmologica. 1998;212(5):328-30. [Medline].
80. Sankaridurg PR, Sharma S, Willcox M, et al. Colonization of hydrogel lenses with Streptococcus pneumoniae: risk of development of corneal infiltrates. Cornea. May 1999;18(3):289-95. [Medline].
81. Schein OD, Buehler PO, Stamler JF, et al. The impact of overnight wear on the risk of contact lens-associated ulcerative keratitis. Arch Ophthalmol. Feb 1994;112(2):186-90. [Medline].
82. Schein OD, Glynn RJ, Poggio EC, et al. The relative risk of ulcerative keratitis among users of daily-wear and extended-wear soft contact lenses. A case-control study. Microbial Keratitis Study Group. N Engl J Med. Sep 21 1989;321(12):773-8. [Medline].
83. Sebag J, Albert DM. Pseudochalazion of the upper lid due to hard contact lens embedding -- case reports and literature review. Ophthalmic Surg. Aug 1982;13(8):634-6. [Medline].
84. Sendele DD, Kenyon KR, Mobilia EF, et al. Superior limbic keratoconjunctivitis in contact lens wearers. Ophthalmology. Jun 1983;90(6):616-22. [Medline].
85. Setala K, Vasara K, Vesti E, Ruusuvaara P. Effects of long-term contact lens wear on the corneal endothelium. Acta Ophthalmol Scand. Jun 1998;76(3):299-303. [Medline].
86. Sheldon L, Biedner B, Geltman C, Sachs U. Giant papillary conjunctivitis and ptosis in a contact lens wearer. J Pediatr Ophthalmol Strabismus. Mar-Apr 1979;16(2):136-7. [Medline].
87. Srinivasan BD, Jakobiec FA, Iwamoto T, DeVoe AG. Giant papillary conjunctivitis with ocular prostheses. Arch Ophthalmol. May 1979;97(5):892-5. [Medline].
88. Stapleton F, Willcox MD, Morris CA, Sweeney DF. Tear changes in contact lens wearers following overnight eye closure. Curr Eye Res. Feb 1998;17(2):183-8. [Medline].
89. Stehr-Green JK, Bailey TM, Visvesvara GS. The epidemiology of Acanthamoeba keratitis in the United States. Am J Ophthalmol. Apr 15 1989;107(4):331-6. [Medline].
90. Stern GA. Contact lens associated bacterial keratitis: past, present, and future. CLAO J. Jan 1998;24(1):52-6. [Medline].
91. Sugar A, Meyer RF. Giant papillary conjunctivitis after keratoplasty. Am J Ophthalmol. Feb 1981;91(2):239-42. [Medline].
92. Talamo JH, Larkin DS. Bilateral Acanthamoeba keratitis and gas-permeable contact lenses. Am J Ophthalmol. Nov 15 1993;116(5):651-2. [Medline].
93. Vallas V, Stapleton F, Willcox MD. Bacterial invasion of corneal epithelial cells. Aust N Z J Ophthalmol. Jun-Aug 1999;27(3-4):228-30. [Medline].
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