Key Features
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Overall safety record of contact lenses is excellent.
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Low-Dk lenses, overnight wear, and poor lens care practices are modifiable risk factors for the development of contact lens–related problems.
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Patient education remains an important avenue for prevention of complications of contact lens wear.
Introduction
In the United States, an estimated 40.9 million adults wear contact lenses, and nearly one third of them have experienced a contact lens–related complication requiring a visit to their doctors. Although many contact lenses are managed by optometrists and opticians, some complications threaten sight and the long-term health of the eye, which makes it important that ophthalmologists are well informed about this problem. This chapter will discuss toxic and allergic reactions, conditions reflecting metabolic challenge, corneal inflammatory events (CIEs), and microbial keratitis (MK). The long-term sequelae of these contact lens–related complications range from mild, self-limiting disease to vision loss even with proper treatment. Problems related to fit, comfort, and tolerance, including lens warpage, tight lens, dry eye, deposits, and mucin balls, are outside the scope of this chapter.
Toxic, Allergic and Mechanical Reactions
Solutions
Toxic or allergic conjunctivitis may be caused by some components of the lens care system. The agents frequently responsible for toxic or allergic reactions are preservatives, disinfectants, surfactant and enzyme cleaners, and concentrated hydrogen peroxide. Allergic reactions are hypersensitivity reactions that occur after repeated exposure to the sensitizing antigen. In the past, thimerosal was a common offender, but sorbate and benzalkonium chloride are likely causes now.
Patients with a toxic reaction experience immediate ocular discomfort and conjunctival injection with lens insertion. Toxic conjunctivitis can occur the first time the solution is used or may result from a buildup of the toxic component in the hydrogel material. Typically, patients have used the care system for 1 month or longer before symptoms of conjunctival injection and irritation develop. On examination, conjunctival hyperemia, follicles, superficial punctate keratitis, scattered fine infiltrates, and superior limbic keratoconjunctivitis may be seen ( Fig. 4.24.1 ). Discontinuation of the solution results in resolution of symptoms, but if the symptoms and signs are severe, a short course of topical corticosteroids may be needed. When resuming lens wear, wearers of hydrogel lenses should replace their lenses, which may have absorbed the offending agent, but wearers of rigid gas-permeable (RGP) lenses may use the same lenses if they are thoroughly cleaned and rinsed. Incorrect use of solutions and cleaners can contribute to toxic reactions, especially with incomplete rinsing of surfactant cleaners or failure to neutralize peroxide solutions. Environmental chemical exposure, such as cosmetics and hair sprays, may also lead to toxic or allergic reactions when they contaminate lenses. Patients can be switched to care systems with different preservatives or to daily disposable lenses to avoid solutions altogether.
There have been case reports of severe toxic reactions to contact lens use that resemble central toxic keratopathy syndrome—a constellation of corneal thinning and flattening, hyperopic shift, and marked stromal “mud crack” central opacity. Treatment includes removal of the offending chemicals; use of preservative-free solutions; topical corticosteroid, if inflammation is severe; and a change to more frequent lens replacement and/or alternative lens material and care system.
Giant Papillary Conjunctivitis
Giant papillary conjunctivitis (GPC), sometimes called contact lens papillary conjunctivitis (CLPC), was first reported in the 1970s and is thought to be a result of both mechanical irritation and immunological stimulation. It is believed that a cell-mediated reaction to the antigens deposited on contact lenses causes trauma to the tarsal conjunctiva, exposing the antigens to the ocular immune system and initiating the reaction. It should be noted that GPC has also been reported in those who do not wear contact lenses as a result of other causes of mechanical irritation, such as exposed sutures, extruded scleral buckles, foreign bodies, cyanoacrylate glue, ocular prostheses, and filtering blebs. GPC is characterized by itching, burning, increased mucus production, foreign-body sensation, and papillae on the upper tarsus ranging from 0.3–2 mm ( Figs. 4.24.2, 4.24.3, 4.24.4 ). It is the most common complication of contact lens use. Patients typically report increased deposits on lenses, which may be visible on examination. Papillae are a late finding and are not necessary for diagnosis.
Factors associated with GPC include duration of wear, hygiene, history of atopy/environmental allergy, and the fall and spring seasons. Lens cornea fit, bacterial bioburden, history of adverse ocular events, race, and gender are not associated with GPC.
The initial treatment for GPC is removal of the inflammatory stimulus via cessation of contact lens wear for 2–4 weeks. When resuming use, it may be helpful to decrease wear time, institute more frequent lens replacement, optimize lens hygiene with goal of reducing deposits, or prescribe a new lens material or design. Limited wear of daily disposable lenses is a good way of reintroducing lens wear while minimizing antigen presentation. Adjunctive therapies for severe cases include topical mast cell stabilizers, used as initial treatment and for suppressive maintenance, and pulse regimen of topical corticosteroid, with appropriate monitoring. The role of topical immunomodulators, such as tacrolimus, has been reported. GPC is not vision threatening, and with proper management, resolution of redness and discharge is typically expected within 1–2 weeks. When inflammation is severe or long-standing, the papillae may remain.
Superior Limbic Keratoconjunctivitis
Contact lens wear has been associated with injection and fluorescein staining of the superior bulbar conjunctiva, termed superior limbic keratoconjunctivitis (SLK). Patients may experience tearing, burning, foreign body sensation, and lens intolerance. The appearance is similar to idiopathic SLK described by Theodore in 1963, which, interestingly, is sometimes treated with therapeutic lenses. SLK in contact lens wearers has been associated with preservatives in contact lens solutions, but mechanical irritation from poor-fitting contact lenses may also be a factor.
In contact lens–associated SLK, the superior corneal epithelium is irregular with a micropannus and punctate staining ( Fig. 4.24.5 ). A papillary reaction is often present on the superior tarsal conjunctiva, but the papillae tend to be smaller than those seen in GPC. Discontinuation of lens wear and topical lubrication is generally effective, but resolution may take weeks or months. Punctal occlusion may aid in resolution of symptoms. Patients can return to lens wear after being refitted with new lenses and switching to hydrogen peroxide disinfection, and nonpreserved saline daily disposable lenses are another option for SLK patients
Solutions
Toxic or allergic conjunctivitis may be caused by some components of the lens care system. The agents frequently responsible for toxic or allergic reactions are preservatives, disinfectants, surfactant and enzyme cleaners, and concentrated hydrogen peroxide. Allergic reactions are hypersensitivity reactions that occur after repeated exposure to the sensitizing antigen. In the past, thimerosal was a common offender, but sorbate and benzalkonium chloride are likely causes now.
Patients with a toxic reaction experience immediate ocular discomfort and conjunctival injection with lens insertion. Toxic conjunctivitis can occur the first time the solution is used or may result from a buildup of the toxic component in the hydrogel material. Typically, patients have used the care system for 1 month or longer before symptoms of conjunctival injection and irritation develop. On examination, conjunctival hyperemia, follicles, superficial punctate keratitis, scattered fine infiltrates, and superior limbic keratoconjunctivitis may be seen ( Fig. 4.24.1 ). Discontinuation of the solution results in resolution of symptoms, but if the symptoms and signs are severe, a short course of topical corticosteroids may be needed. When resuming lens wear, wearers of hydrogel lenses should replace their lenses, which may have absorbed the offending agent, but wearers of rigid gas-permeable (RGP) lenses may use the same lenses if they are thoroughly cleaned and rinsed. Incorrect use of solutions and cleaners can contribute to toxic reactions, especially with incomplete rinsing of surfactant cleaners or failure to neutralize peroxide solutions. Environmental chemical exposure, such as cosmetics and hair sprays, may also lead to toxic or allergic reactions when they contaminate lenses. Patients can be switched to care systems with different preservatives or to daily disposable lenses to avoid solutions altogether.
There have been case reports of severe toxic reactions to contact lens use that resemble central toxic keratopathy syndrome—a constellation of corneal thinning and flattening, hyperopic shift, and marked stromal “mud crack” central opacity. Treatment includes removal of the offending chemicals; use of preservative-free solutions; topical corticosteroid, if inflammation is severe; and a change to more frequent lens replacement and/or alternative lens material and care system.
Giant Papillary Conjunctivitis
Giant papillary conjunctivitis (GPC), sometimes called contact lens papillary conjunctivitis (CLPC), was first reported in the 1970s and is thought to be a result of both mechanical irritation and immunological stimulation. It is believed that a cell-mediated reaction to the antigens deposited on contact lenses causes trauma to the tarsal conjunctiva, exposing the antigens to the ocular immune system and initiating the reaction. It should be noted that GPC has also been reported in those who do not wear contact lenses as a result of other causes of mechanical irritation, such as exposed sutures, extruded scleral buckles, foreign bodies, cyanoacrylate glue, ocular prostheses, and filtering blebs. GPC is characterized by itching, burning, increased mucus production, foreign-body sensation, and papillae on the upper tarsus ranging from 0.3–2 mm ( Figs. 4.24.2, 4.24.3, 4.24.4 ). It is the most common complication of contact lens use. Patients typically report increased deposits on lenses, which may be visible on examination. Papillae are a late finding and are not necessary for diagnosis.
Factors associated with GPC include duration of wear, hygiene, history of atopy/environmental allergy, and the fall and spring seasons. Lens cornea fit, bacterial bioburden, history of adverse ocular events, race, and gender are not associated with GPC.
The initial treatment for GPC is removal of the inflammatory stimulus via cessation of contact lens wear for 2–4 weeks. When resuming use, it may be helpful to decrease wear time, institute more frequent lens replacement, optimize lens hygiene with goal of reducing deposits, or prescribe a new lens material or design. Limited wear of daily disposable lenses is a good way of reintroducing lens wear while minimizing antigen presentation. Adjunctive therapies for severe cases include topical mast cell stabilizers, used as initial treatment and for suppressive maintenance, and pulse regimen of topical corticosteroid, with appropriate monitoring. The role of topical immunomodulators, such as tacrolimus, has been reported. GPC is not vision threatening, and with proper management, resolution of redness and discharge is typically expected within 1–2 weeks. When inflammation is severe or long-standing, the papillae may remain.
Superior Limbic Keratoconjunctivitis
Contact lens wear has been associated with injection and fluorescein staining of the superior bulbar conjunctiva, termed superior limbic keratoconjunctivitis (SLK). Patients may experience tearing, burning, foreign body sensation, and lens intolerance. The appearance is similar to idiopathic SLK described by Theodore in 1963, which, interestingly, is sometimes treated with therapeutic lenses. SLK in contact lens wearers has been associated with preservatives in contact lens solutions, but mechanical irritation from poor-fitting contact lenses may also be a factor.
In contact lens–associated SLK, the superior corneal epithelium is irregular with a micropannus and punctate staining ( Fig. 4.24.5 ). A papillary reaction is often present on the superior tarsal conjunctiva, but the papillae tend to be smaller than those seen in GPC. Discontinuation of lens wear and topical lubrication is generally effective, but resolution may take weeks or months. Punctal occlusion may aid in resolution of symptoms. Patients can return to lens wear after being refitted with new lenses and switching to hydrogen peroxide disinfection, and nonpreserved saline daily disposable lenses are another option for SLK patients
Conditions Reflecting Metabolic Challenge
Corneal Hypoxia and Edema
Contact lenses create a physical barrier that impairs the cornea’s natural ability to harvest oxygen from the atmosphere and may lead to corneal hypoxia. With continued hypoxia, cell death occurs, leading to erosions or necrosis and desquamation and causing decreased vision, pain, tearing, and photoallodynia. Chronic low-grade hypoxia causes subtle changes in corneal physiology and structure. Examination findings may include central epithelial microcysts and edema (“Sattler’s veil”), neovascularization ( Fig. 4.24.6 ), stromal thickening and striae, and endothelial blebs ( Fig. 4.24.7 ). The corneal edema can fluctuate throughout the day, typically being worse in the morning. Lens wear should be discontinued until the edema resolves and then a high-Dk lens should be substituted.
Neovascularization
As previously mentioned, chronic low-grade hypoxia can cause corneal neovascularization. Hypoxia results in the accumulation of lactic acid and carbon dioxide, which stimulates vascular ingrowth and hypoxic dilation of limbal vessels. Although typically associated with low-Dk hydrogel lenses, neovascularization may also be seen with poorly fit RGP lenses because of chronic irritation, such as in vascularized limbal keratitis (VLK). VLK lesions appear as an elevated, opaque mass at the limbal–epithelial junction with superficial and deep vascularization.
Superficial neovascular changes (pannus) are common in patients wearing soft, low-Dk lenses, and may be acceptable if the pannus is stable and it extends less than 1.5 mm onto the cornea. This superficial neovascularization is likely caused by angiogenic factors released in response to chronic limbal trauma and hypoxia. Vascular ingrowth into the corneal stroma is more worrisome because these vessels can lead to lipid exudation, scarring, and intracorneal hemorrhages ( Fig. 4.24.8 ). Stromal neovascular changes or superficial neovascularization that extends more than 2 mm onto the cornea should be considered abnormal and unacceptable. When the patient is refitted with high-Dk lenses, reduction of the abnormal vessels and limbal erythema is expected.
Limbal Stem Cell Deficiency
Limbal stem cell deficiency (LSCD) is caused by the loss of function of corneal epithelial cell precursors. Contact lens–associated LSCD was first referred to as contact lens–induced keratopathy (CLIK), in which the keratoconjunctivitis progressed to diffuse corneal scarring and vascularization, sometimes requiring penetrating keratoplasty. Bowman’s membrane is damaged and replaced by fibrous scar tissue with deep stromal vascularization ( Fig. 4.24.9 ).
The clinical picture of contact lens–induced LSCD is typically milder than other causes of LSCD as evidenced by the finding that 71.4% of patients with contact lens–induced LSCD are asymptomatic. The slit-lamp exam in contact lens–induced LSCD demonstrates whorl-like epitheliopathy, conjunctivalization of the cornea, absence of palisades of Vogt, and late fluorescein staining. As the disease progresses, findings include pannus, epithelial defects, scarring, and vision loss. Treatment of contact lens–induced LSCD depends largely on the severity of disease. Initial medical treatment includes discontinuation of wear and optimization of the tear film and ocular surface via a combination of artificial tears, topical corticosteroid, topical cyclosporine, topical vitamin A, punctal occlusion, and oral doxycycline. If maximal medical therapy fails, surgical options include mechanical removal of conjunctivalized corneal epithelium, amniotic membrane transplantation, and limbal autograft or allogenic transplantation.
Abrasions
Corneal abrasions are epithelial defects caused by trauma to the ocular surface. Abrasions frequently occur with contact lens use during the insertion or removal process and are caused by fingernails or the lens itself. Abrasions allow bacteria access to the corneal stroma, and therefore careful evaluation for MK is warranted when there is an abrasion in the context of contact lens wear. In the setting of contact lens use, recommended treatment of corneal abrasion is a broad-spectrum antibiotic, such as a fluoroquinolone or aminoglycoside, which offers prophylaxis against Pseudomonas. Patching and topical corticosteroids have no proven benefit and should not be used in contact lens–associated corneal abrasions.
Corneal Hypoxia and Edema
Contact lenses create a physical barrier that impairs the cornea’s natural ability to harvest oxygen from the atmosphere and may lead to corneal hypoxia. With continued hypoxia, cell death occurs, leading to erosions or necrosis and desquamation and causing decreased vision, pain, tearing, and photoallodynia. Chronic low-grade hypoxia causes subtle changes in corneal physiology and structure. Examination findings may include central epithelial microcysts and edema (“Sattler’s veil”), neovascularization ( Fig. 4.24.6 ), stromal thickening and striae, and endothelial blebs ( Fig. 4.24.7 ). The corneal edema can fluctuate throughout the day, typically being worse in the morning. Lens wear should be discontinued until the edema resolves and then a high-Dk lens should be substituted.
Neovascularization
As previously mentioned, chronic low-grade hypoxia can cause corneal neovascularization. Hypoxia results in the accumulation of lactic acid and carbon dioxide, which stimulates vascular ingrowth and hypoxic dilation of limbal vessels. Although typically associated with low-Dk hydrogel lenses, neovascularization may also be seen with poorly fit RGP lenses because of chronic irritation, such as in vascularized limbal keratitis (VLK). VLK lesions appear as an elevated, opaque mass at the limbal–epithelial junction with superficial and deep vascularization.
Superficial neovascular changes (pannus) are common in patients wearing soft, low-Dk lenses, and may be acceptable if the pannus is stable and it extends less than 1.5 mm onto the cornea. This superficial neovascularization is likely caused by angiogenic factors released in response to chronic limbal trauma and hypoxia. Vascular ingrowth into the corneal stroma is more worrisome because these vessels can lead to lipid exudation, scarring, and intracorneal hemorrhages ( Fig. 4.24.8 ). Stromal neovascular changes or superficial neovascularization that extends more than 2 mm onto the cornea should be considered abnormal and unacceptable. When the patient is refitted with high-Dk lenses, reduction of the abnormal vessels and limbal erythema is expected.
Limbal Stem Cell Deficiency
Limbal stem cell deficiency (LSCD) is caused by the loss of function of corneal epithelial cell precursors. Contact lens–associated LSCD was first referred to as contact lens–induced keratopathy (CLIK), in which the keratoconjunctivitis progressed to diffuse corneal scarring and vascularization, sometimes requiring penetrating keratoplasty. Bowman’s membrane is damaged and replaced by fibrous scar tissue with deep stromal vascularization ( Fig. 4.24.9 ).
The clinical picture of contact lens–induced LSCD is typically milder than other causes of LSCD as evidenced by the finding that 71.4% of patients with contact lens–induced LSCD are asymptomatic. The slit-lamp exam in contact lens–induced LSCD demonstrates whorl-like epitheliopathy, conjunctivalization of the cornea, absence of palisades of Vogt, and late fluorescein staining. As the disease progresses, findings include pannus, epithelial defects, scarring, and vision loss. Treatment of contact lens–induced LSCD depends largely on the severity of disease. Initial medical treatment includes discontinuation of wear and optimization of the tear film and ocular surface via a combination of artificial tears, topical corticosteroid, topical cyclosporine, topical vitamin A, punctal occlusion, and oral doxycycline. If maximal medical therapy fails, surgical options include mechanical removal of conjunctivalized corneal epithelium, amniotic membrane transplantation, and limbal autograft or allogenic transplantation.
Abrasions
Corneal abrasions are epithelial defects caused by trauma to the ocular surface. Abrasions frequently occur with contact lens use during the insertion or removal process and are caused by fingernails or the lens itself. Abrasions allow bacteria access to the corneal stroma, and therefore careful evaluation for MK is warranted when there is an abrasion in the context of contact lens wear. In the setting of contact lens use, recommended treatment of corneal abrasion is a broad-spectrum antibiotic, such as a fluoroquinolone or aminoglycoside, which offers prophylaxis against Pseudomonas. Patching and topical corticosteroids have no proven benefit and should not be used in contact lens–associated corneal abrasions.
Corneal Inflammatory Events and Microbial Keratitis
There is lack of standardization in the literature and discourse surrounding corneal opacities with or without an overlying defect. It is common for the terms ulcer , infiltrate , sterile infiltrate , presumed microbial keratitis , and so on to be used imprecisely; the authors of this chapter will therefore use a classification system first proposed by Efron et al. This system separates the spectrum of clinical findings into two distinct entities: CIEs and MK.
CIEs include an epithelial or subepithelial infiltrate, with or without an epithelial defect, which improves in the absence of treatment and typically does not cause scarring. Treatment of CIEs may be hastened by antibiotics and/or corticosteroids. However, MK is an epithelial defect with stromal involvement or tissue loss (also referred to as “crater”), typically leaves a scar, has a presumed or confirmed pathogen and requires intensive treatment with antimicrobials. It is acceptable to use the term “ulcer” when referring to MK but not to CIEs.
The Role of Lens Care Systems
For several years, multipurpose solutions (MPSs) have been the most popular lens care products. They may contain surfactant cleaners, disinfecting agents, preservatives, and polymers or conditioners to make the contact lens more comfortable. The disinfecting component must contain antimicrobial agents sufficient to destroy micro-organisms. Despite approval by the U.S. Food and Drug Administration (FDA) and the popularity of MPS solutions, recent outbreaks of MK have focused attention on lens care. Studies also suggest other problems with MPS care systems because some solutions can, in fact, increase the binding of Pseudomonas to epithelial cells and decrease the rate of epithelial cell exfoliation. Polyhexamethylene biguanide (PHMB)–based systems used with FDA group II lenses (high water, nonionic) resulted in increased corneal staining, and biguanides used with group IV lenses (high water, ionic) also increased staining and decreased biocide efficacy. Lens wearers with solution-associated corneal staining were significantly more likely to develop corneal infiltrates. In general, hydrogen peroxide care systems appear to have the best profile for disinfection of lenses and the lowest incidence of CIEs and corneal staining.
In addition, lens handling greatly increases the incidence of lens contamination, with more than half the lenses removed aseptically from the eye showing microbial contamination. Studies have shown that greater than 50% of lens cases are contaminated. All types of care solutions can become contaminated, including up to 30% of preserved solutions. Not surprisingly, those who wear contact lenses infrequently had a higher contamination rate. Rinsing lenses with saline or MPS appears to be effective in reducing contamination. Use of daily disposable lenses is a way to avoid contamination and is associated with lower complication rates compared with other modes of daily soft lens wear.
Corneal Inflammatory Events
Contact lens–related CIEs range from small, asymptomatic lesions to large opacities that obscure vision. The opaque lesions are caused by polymorphonuclear and mononuclear leukocyte recruitment to the cornea and are likely host response to commensal organisms or lens-related bacteria. Bacteria can form a biofilm on the surface of the lens or the lens case, and one study found that more than 70% of the risk for CIEs was related to the exposure to the lens biofilm. Multiple other causes, including hypoxia, retrolental debris, and staphylococcal immune complexes, have been proposed and investigated. The epithelium is usually intact but may show overlying superficial punctate keratitis, and the anterior chamber shows only minimal reaction. Symptoms typically include irritation, pain, foreign body sensation, photoallodynia, and tearing.
The true incidence and significance of peripheral infiltrates is an area of ongoing study and debate. Sankaridurg et al. found that 1.6% of asymptomatic patients with no history of contact lens wear had corneal infiltrates at the start of a study comparing spectacle wear and daily disposable lenses. Asymptomatic infiltrates were seen in spectacle wearers at a rate of 11.3 events per 100 years of wear compared with 20.5 events per 100 years in wearers of daily disposable lenses. The daily disposable group had 2.5 symptomatic peripheral ulcers events, but no events were noted in the spectacle group. Several other studies have reported the incidence of sterile peripheral infiltrates in users of extended-wear disposable lenses to be equal to or higher than daily wear.
A large study of 6245 lens wearers found lens-related CIE in 159 patients (2.5%). Risk factors included age ≤25 years or less and greater than 50 years; refractive error greater than +5.00 diopters (D); smoking; and failure to maintain prescribed wear schedule. Further, a meta-analysis of published and presented studies (1991–2006) found a twofold higher risk for CIEs in users of SH lenses worn for up to 30 days compared with low-Dk extended-wear lenses worn for 7 days. However, it was not clear if the increased risk was related to the lens material or the wear schedule.
The Moorfields Eye Hospital (London, UK) compared daily disposable, silicone hydrogel, and planned replacement lenses and found a significantly reduced risk of toxic/hypersensitivity reactions, papillary conjunctivitis, and metabolic disorders for daily disposables but an increased risk of sterile keratitis and mechanical disorders. Silicone hydrogels did not cause hypoxic complications but had an increased risk of sterile keratitis, mechanical disorders, and nonulcerative complications compared to conventional soft lenses. Risk factors for CIEs included overnight wear, more days of lens wear per week, poor hand hygiene, smoking, and inexperience with use. The authors concluded neither daily disposable lenses nor silicone hydrogels reduced the overall risk of acute nonulcerative events. Corneal scrape and cultures can be obtained to evaluate for infectious etiologies and should especially be acquired if the infiltrate increases, vision is affected, or if the infiltrate is large (>1 mm). However, it is difficult to rely only on culture data to guide clinical decision making. Reported cultures of “obvious” MK are positive 43%–86% of the time, yet one study of “sterile” peripheral infiltrates found positive cultures in 50% of the subset of patients. Many clinicians believe that small peripheral infiltrates do not require cultures, but cultures on organisms have been performed, particularly if an epithelial defect is present. When organisms are recovered, they tend to be less virulent than those associated with central ulcers. The most common isolate is staphylococcus spp., but even in the face of positive culture results, many authors believe that peripheral infiltrates are inflammatory because microorganisms are not recovered in most studies, and infiltrates often resolve with corticosteroid therapy alone.
Discontinuation of lens wear is the first step in the treatment of CIEs. Depending on location and size of the infiltrate and the capacity for monitoring additional treatment options include topical, broad-spectrum antibiotics, topical corticosteroids, or a combination of the two. The clinical appearance can change rapidly, and most patients are seen in 24 hours with modification of therapy, as needed. After resolution, assessment of the patient’s wear and replacement schedules, as well as their care regimen, should be made. Extended wear should be discouraged. Reduction of bioburden at the lid margins and in lens cases, as well as a switch to daily disposable or hydrogen peroxide care system, should be considered.
Microbial Keratitis
Although the overall incidence is low, contact lens wear is now considered the major risk factor for MK, with about 65% of all new ulcers related to contact lens use. MK can be sight threatening because of corneal scarring and is therefore important to differentiate early-stage MK from CIEs so as to not delay treatment.
The most important risk factor for MK is overnight or extended lens use, followed by poor lens/lens case disinfection, smoking, lower socioeconomic class, and failure to wash hands. It is surprising that the surge in disposable single-use contact lenses has not decreased the rates of MK; however, there has been a decrease in vision loss caused by MK in daily contact lens wearers. Stapleton reported a higher incidence rate of MK with silicone hydrogel (SH) contact lenses compared to daily disposable, and higher rates of MK when SH contact lenses were worn overnight compared with conventional hydrogels. Overall, daily disposable lenses are associated with less severe MK and are less likely to cause vision-impairing central MK.
Findings associated with MK include positive corneal culture results, continuous pain after discontinuation of wear, photoallodynia, purulent discharge ( Fig. 4.24.10 ), conjunctival injection, epithelial staining, anterior chamber reaction and corneal edema that surrounds an infiltrate. Stromal opacities in MK are usually larger than 1.5 mm and have overlying epithelial defect and purulent discharge. Multiple studies have demonstrated that pathogenic microorgranisms, especially Pseudomonas spp., fungi, Acanthamoeba , and Nocardia , are the main causes and determinants of outcome in MK.
