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Complications of contact lenses

Complications of contact lenses
Literature review current through: Sep 2023.
This topic last updated: Feb 08, 2023.

INTRODUCTION — Millions of people worldwide wear contact lenses. Noninfectious and infectious complications of contact lenses are common and vary in severity from clinically inconsequential to potentially vision-threatening. In a survey of contact lens wearers in the United States, nearly one-third had experienced a contact lens-related condition that required a doctor's visit [1].

Primary care and emergency department clinicians are often the first to evaluate patients with contact lens-related problems. Although many of these conditions necessitate referral to an eye care specialist, familiarity with these complications by the frontline clinician will allow prompt diagnosis, treatment, and appropriate triage.

The presentation and management of complications associated with contact lenses will be reviewed here. An overview of contact lenses and specific microbial infections related to contact lens wear are discussed separately. (See "Overview of contact lenses" and "Clinical manifestations and diagnosis of Fusarium infection", section on 'Keratitis' and "Free-living amebas and Prototheca", section on 'Keratitis'.)

NONINFECTIOUS COMPLICATIONS — The maintenance of a smooth and transparent anterior refractive surface is critical to good vision. A complex interplay between the corneal and conjunctival epithelium, the tear film, and the overlying eyelids provides protection against infection and scarring. Noninfectious complications are minimized with a well-fit contact lens that both rests on the precorneal tear film and moves only enough to allow good fluid and gas exchange, thereby functioning as a de facto extension of the ocular surface.

Dryness — Contact lens-related dryness is commonly encountered and is the most frequent reason for contact lens discontinuation. Dryness can be caused by poor tear film, material, water content, wearing modality/replacement schedule, oxygen deprivation, lens deposits, environmental factors, and contact lens solution incompatibility [2-11]. Treatment includes artificial tears with and without contact lenses, topical cyclosporine and lifitegrast, and management of blepharitis and meibomian gland dysfunction when applicable. Patients may benefit from using lubricant eye drops before and after contact lens wear [12], refitting with a higher oxygen-permeable lens material, or switching contact lens care solutions. (See "Dry eye disease" and "Blepharitis".)

Sterile corneal infiltrates — Multiple small infiltrates containing inflammatory cells (polymorphonuclear leukocytes and mononuclear cells) may accumulate within the collagen matrix of the corneal stroma in people who wear contact lenses [13]. These infiltrates appear white and are located in the anterior stroma, usually in the peripheral cornea near the limbus (picture 1). They can occur singly or in clusters and are usually 0.1 to 1.0 mm in size. The infiltrates may be difficult to see without slit lamp biomicroscopy.

Sterile infiltrates are usually asymptomatic but can cause pain, discomfort, tearing, or photophobia if they are severe or numerous. In many cases, the diagnosis is made during routine eye examination in contact lens wearers.

The infiltrates are believed to result from a number of insults associated with contact lens wear: accumulated debris, chemical toxicity, hypoxia, and hypersensitivity and overnight wear (extended wear). Risks factors include years of lens wear, use of multipurpose care products, silicone hydrogel lenses, patient age, and extended wear of lenses [14-18].

The infiltrates may also represent an immune reaction to exotoxins from staphylococci colonizing the sebaceous gland openings of the eyelid margins (staphylococcal marginal keratitis). (See "Blepharitis", section on 'Classification and pathophysiology'.)

Ophthalmology consultation is appropriate to distinguish these infiltrates from infection and to initiate topical corticosteroids when indicated. Sterile infiltrates respond well to a short course of topical corticosteroids or, in many patients, temporary elimination of contact lens wear. Concomitant control of the ocular surface and eyelid bacterial flora over a course of weeks may also be beneficial. This may involve eyelid hygiene, topical antibiotics, oral omega-3 fatty acid supplements, or oral doxycycline 50 to 100 mg once or twice daily [19]. (See "Blepharitis", section on 'Management'.)

Corneal epithelial problems — Contact lenses may cause defects of the corneal epithelium through mechanical trauma, oxygen deprivation, nutrient starvation, metabolic injury, hypersensitivity, drying, or chemical toxicity. Epithelial defects of the cornea can be seen by staining the eye with fluorescein dye. The dye is taken up by discontinuity of the epithelial surface related to cell damage or death.

Mild staining of the epithelium is common, usually asymptomatic, and of little clinical consequence. Larger defects may cause pain, tearing, red eyes (conjunctival injection), photophobia, and blurred vision.

Superficial punctate staining of the epithelium may be caused by a poorly fit lens (eg, too steep or flat), hypoxia, chemical toxicity from storage or cleaning solutions, lens deposits, blepharitis, dry eyes, or desiccation from poor eyelid closure. Significant defects are usually the result of mechanical trauma in the form of an abrasion to the epithelial surface that is rendered more susceptible to denudation by the overall stress of contact lens wear.

Microcysts in the epithelial layer may result from pockets of dead cellular debris associated with hypoxia in extended wear contact lens users [20]. These microcysts appear as small, scattered, white dots by slit lamp biomicroscopy [20]. Although treatment is not indicated in most patients, severe or persistent cases may necessitate switching to daily wear contact lenses or to eliminating contact lens wear.

Mechanical corneal abrasion — The contact lens is essentially a foreign body that is retained in the eye for hours or weeks with repetitive pressing and sliding on the cornea with each blink. Mechanical abrasions can result from traumatic insertion and removal of the lens; tears, scratches, or chips in the lens; or foreign debris trapped under the lens. Abrasions are typically very painful because the superficial cornea is replete with sensory nerve endings (see "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis"). Torn, scratched, or chipped contact lenses may also cause abrasion and discomfort.

Corneal abrasions related to contact lens wear pose a risk for bacterial ulcerative keratitis. As a result, preventive therapy is indicated with antibiotics effective against Pseudomonas, such as ofloxacin, ciprofloxacin, or tobramycin. Sulfacetamide and erythromycin are not satisfactory choices because they do not provide adequate Pseudomonas coverage. The antibiotics should be provided as eye drops used four times daily. More frequent instillation may delay healing through toxic effects [21].

Lens wear should be discontinued and the patient advised to use cold compresses and oral nonsteroidal antiinflammatory drugs (NSAIDs) for pain management. Cycloplegia may also provide pain relief [22]. Close follow-up should be provided at 24 hours and through five days after the injury.

Patching contact lens patients as a treatment for a corneal abrasion is contraindicated due to high risk of secondary infection. A meta-analysis of 11 randomized trials of patients with simple corneal abrasions (less than 10 mm diameter and not all related to contact lens wear) found that patching did not hasten the epithelialization process or improve patient comfort [23]. In addition, patching worsens the condition if an apparent contact lens-related corneal abrasion actually represents an early Pseudomonas ulcer prior to development of clinically visible infectious infiltrates [21]. (See 'Initial management' below and "Corneal abrasions and corneal foreign bodies: Management".)

Hypoxic reactions — The cornea derives its oxygen by direct diffusion from the ocular surface. The presence of a contact lens, if not freely permeable to gas, may reduce access to oxygen. Hypoxia is worse at night under the closed eyelids in extended wear contact lens wearers.

Hypoxia results in microcystic edema and punctate staining of the corneal epithelium, stromal edema (manifested by a steamy, cloudy, and thickened cornea with striae or folds in the Descemet membrane), decreased visual acuity, photophobia, and conjunctival hyperemia. Chronic hypoxia may lead to superficial and, rarely, deep corneal neovascularization, especially at the superior limbus [24]. Patients who experience contact lens-related hypoxia may benefit by switching to a higher oxygen-permeable lens material [25].

Toxic and/or immune reactions — Chemicals in contact lens solutions may produce toxic or immune reactions on the corneal epithelium in susceptible individuals. Such reactions may result in severe, diffuse superficial punctate epitheliopathy (picture 2), frank epithelial erosion and defects, pseudodendrites, and conjunctival hyperemia. The multiple, small subepithelial corneal infiltrates resulting from chemical toxicity may be mistaken for viral infiltrates.

Contact lens disinfection systems comprised of biocides, surfactants, wetting agents, and chelating agents have been implicated [26,27]. The preservative thimerosal, now rarely used, was at one time frequently responsible for toxic and immune keratoconjunctivitis.

Undiluted enzyme cleaner and hydrogen peroxide disinfectant may cause a severe acute keratitis. Hydrogen peroxide-based care systems may cause gas bubble formation in the epithelium and cause temporary loss of vision. Commercial multipurpose contact lens solutions contain more dilute concentrations of enzyme and hydrogen peroxide and are therefore safer than older preparations.

Central toxic keratopathy, seen in patients after refractive surgery, has been reported in patients after extended contact lens wear. Central toxic keratopathy is characterized by central corneal opacification, thinning, and hyperopic shift. Confocal microscopy shows edema and rearrangement of collagen fibrils with cellular infiltration and interspersed refractile elements [18,28].

Superior limbic keratoconjunctivitis — A condition resembling superior limbic keratoconjunctivitis (SLK) [29] may be seen in some contact lens wearers [30,31]. Classic SLK, associated with dry eye syndrome or autoimmune thyroid disease, presents as tearing, burning, a foreign body sensation, mild photophobia, and mucous discharge. There is a thickened, keratinized, and hyperemic superior bulbar and palpebral conjunctiva (picture 3). Rose-Bengal or lissamine green dye staining reveals superior corneal and conjunctival punctate staining. The central cornea is not involved. Superior filamentary keratitis and papillary keratopathy are also commonly seen.

Contact lens wear (almost exclusively with soft lenses) may result in many of the manifestations of SLK. However, filamentary keratitis is absent and the keratitis may extend to the central cornea, resulting in decreased visual acuity. The symptoms resolve upon cessation of contact lens wear, but the corneal and conjunctival changes may persist for months to years. Treatment consists of eliminating lens wear until the ocular surface returns to normal or switching to rigid gas-permeable lenses. Glucocorticoid treatment is of minimal benefit.

Tight lens syndrome — Contact lenses normally ride on a layer of tears that allows adequate lens movement and oxygen diffusion. A lens that adheres too tightly to the corneal surface functions like a suction cup and may cause severe pain, blurred vision, redness, and photophobia. The contact lens is immobile and difficult to remove.

The tight lens syndrome may cause corneal epithelial staining, marked corneal stromal edema with small peripheral infiltrates, an anterior chamber inflammatory reaction, and severe conjunctival hyperemia. The signs and symptoms resolve within a few days of removal of the contact lens. A short course of artificial tears and topical corticosteroids may hasten resolution of the clinical manifestations.

Contact lens removal may be facilitated by applying a topical anesthetic and contact lens saline solution before attempting to slide the lens off to the side or by using a suction-plunger lens remover designed for removal of rigid lenses (picture 4).

Dislocated contact lens — A contact lens may become dislodged from the cornea, migrate under the upper eyelid, and become embedded in the tissues of the superior cul-de-sac (fornix), causing pain, irritation, redness, and eyelid swelling [32]. This condition occurs more commonly with rigid contact lenses but can be due to torn or folded soft contact lenses.

Chronic dislocation (over weeks to months) occasionally produces sterile abscesses, cysts, eyelid retraction, orbital masses, foreign body granulomas, ptosis, and subconjunctival embedding [33-35]. Extreme ("double") eversion of the upper eyelid may be necessary to locate and remove the problematic lens.

Giant papillary conjunctivitis — Giant papillary conjunctivitis is a noninfectious inflammatory disorder that represents a reaction to lid movement over a foreign substance, such as contact lenses. It can occur in both soft and rigid gas-permeable contact lens wearers and is characterized by foreign body sensation on the upper eyelid, associated with formation of "giant" (>1 mm) papillae (picture 5). Giant papillary conjunctivitis is discussed in detail separately. (See "Giant papillary conjunctivitis".)

Subconjunctival hemorrhage — Subconjunctival hemorrhage is a benign disorder characterized by the acute appearance of a flat area of bleeding under the conjunctiva (picture 6). Subconjunctival hemorrhage can be a complication of contact lens use, occurring in approximately 5 percent of contact lens wearers [36].

Endothelial complications — Chronic hypoxia and acidosis in long-term contact lens wearers may cause permanent morphologic changes, including reduced density of the endothelial cells that line the innermost surface of the cornea [37-39]. These cells pump excess fluid out of the stroma and are crucial in maintaining corneal clarity.

Limbal stem cell deficiency — Awareness of contact lens-induced limbal stem cell deficiency (LSCD) has increased over the past decade. Limbal stem cells, which reside at the basal limbal region, function to maintain and regenerate the corneal epithelium and serve as a barrier to prevent conjunctival epithelium from invading the cornea [40,41]. LSCD can result from chronic trauma and hypoxic injury associated with contact lens wear. Significant ocular morbidity is possible since limbal stem cells do not regenerate. It is estimated that 2.4 to 5 percent of contact lens wearers develop signs of LSCD that correlate with the duration of use [42]. Most cases involve soft contact lenses, although it has been described with other lens types [42-45].

Patients with LSCD report decreased vision, dryness, redness, irritation, photophobia, and pain, although they often remain asymptomatic in the early stages [46]. Clinical manifestations include focal or diffuse abnormal corneal epithelium in a whorl-like pattern with late fluorescein staining, recurrent or persistent epithelial defects, corneal conjunctivalization and neovascularization, subepithelial haze and scarring, ulceration, melting, and even perforation [42,43].

Conservative treatment includes discontinuation of contact lenses and frequent use of preservative-free artificial tears, commonly four times a day or more if feasible. Additional topical treatment options including corticosteroids, cyclosporine, and autologous serum tears can be added depending on the disease severity. For these cases, appropriate clinical decision can be made by referring to an eye care specialist. In more advances cases, mechanical debridement of the irregular epithelium, amniotic membrane grafting, and limbal stem cell auto/allografting may be considered [46-48].

INFECTIOUS KERATITIS — Infectious keratitis is the most serious complication of contact lens use. Contact lens wear is the largest single risk factor for infectious keratitis in the United States [1], although trauma is the largest cause in resource-limited countries, particularly in Asia [49].

Incidence and risk factors — By type of contact lens, annual incidence rates of infectious keratitis have been reported as follows [50]:

Rigid lenses – 0.026 percent

Daily-wear soft lenses – 0.052 percent

Extended-wear soft lenses – 0.18 percent

Contact lens wear may increase the risk of infectious keratitis by several mechanisms. Some of the most common include breakdown of the natural protective barriers of the ocular surface and tear film, entrapment of microorganisms and formation of microbial biofilms on the lens surface, as well as contamination of lenses, storage cases, and disinfecting solutions.

Certain aspects of contact lens use are particularly associated with infectious keratitis:

Type of contact lens – Overnight or extended wear of contact lenses may be associated with a 6- to 15-fold increase in the risk of infectious keratitis [17,51,52]. Infectious keratitis is more common with use of daily wear reusable lenses than daily disposable ones and is least common with use of rigid gas-permeable lenses [53,54].

Lens modality – Daily disposable contact lens wear has been show to have a lower risk of infection severity and vision loss [55]. The risk of corneal infection increases with the number of days per week the lens is worn, and thus has been suggested to be a dose response effect [56].

Lack of input from eye care professional – Obtaining contact lenses without supervision by an eye care professional has been associated with an increased risk for infectious keratitis [57]. These include corrective contact lenses obtained without prescriptions and nonprescription cosmetic lenses [57,58]. The mechanism of increased risk is uncertain but is likely related to poor fit or poor handling and hygiene due to lack of instructions given to the patient.

Lens hygiene – Improper maintenance and wear behaviors contribute to the risk of infectious keratitis. Greater than 80 percent of contact lens users report at least one behavior that put them at risk for a contact lens-related eye infection [59,60]. Examples of poor contact lens practices include:

Wetting the lens in saliva

Reusing multipurpose solution

Failure to use fresh lens care solution with every disinfection cycle (“topping off”)

Failure to rub and rinse lenses when using multipurpose solutions

Preparing solution using saline tablets reconstituted with store-bought distilled water

Not regularly cleaning or replacing the lens storage case

Showering in lenses [61]

Other risk factors include previous eye surgery, lagophthalmos (inability to close the eyelids completely), dry eye, blepharitis, and loss of corneal sensation. Use of ophthalmic or systemic corticosteroids or chemotherapy additionally increase the risk of infection. Smoking has also been recognized as a risk factor [62].

Although most infectious keratitis associated with contact lens use is bacterial, additional risk factors for fungal infections, specifically, include altered host immunity, contact lens use in tropical and semitropical regions of the world, and corneal trauma from organic matter such as wood or while gardening.

Microbiology — Bacterial keratitis comprises 95 percent of all contact lens infections. In referral-based institutions, bacterial infections are predominantly due to Gram-negative organisms, such as Pseudomonas, followed by Gram-positive bacteria (eg, Staphylococcus and Streptococcus) that constitute the normal ocular surface flora [63,64].

Fungi and Acanthamoeba are less common causes of contact lens keratitis, although there are reports of increasing incidence of these pathogens [65], which can lead to severe infection and poor vision outcomes. Diagnosis and treatment of these infections are often delayed because of lower indices of suspicion, relative unfamiliarity, and clinical signs that masquerade as viral or bacterial infection. Amebic and fungal keratitis are discussed in detail separately. (See "Epidemiology, clinical manifestations, and diagnosis of Scedosporium and Lomentospora infections", section on 'Clinical manifestations' and "Clinical manifestations and diagnosis of Fusarium infection", section on 'Immunocompetent patients' and "Treatment and prevention of Fusarium infection", section on 'Keratitis' and "Free-living amebas and Prototheca", section on 'Keratitis'.)

Clinical features — Symptoms and signs of infectious keratitis usually begin within 24 hours of infection. Most patients present with a painful red eye. They may also have reduced visual acuity, eyelid swelling, and photophobia. Corneal defects are evident on fluorescein staining.

The following signs may be present on slit lamp examination:

Yellow or white stromal infiltrates – Bacterial keratitis is often associated with yellow infiltrates while fungal keratitis tends to have white infiltrates, often with feathery borders, spreading branches, and multiple smaller satellite infiltrates (picture 7).

Corneal edema.

Stromal loss and thinning.

Anterior chamber cellular reaction (white blood cells in the anterior chamber).

Hypopyon (layering of white blood cells in the anterior chamber (picture 8).

Fibrin (proteinaceous exudation) in the anterior chamber.

Wessely ring infiltrate (sterile immune infiltrate in the corneal stroma) (picture 9).

Flat anterior chamber, if the cornea is perforated.

Diagnostic approach

Clinical suspicion and evaluation — Infectious keratitis should be suspected in any contact lens wearer who presents with a red, painful eye. The evaluation includes careful history, ophthalmologic examination including fluorescein staining of the eye, and slit lamp examination.

History – Obtaining a history may provide clues to the microbial etiology. Rapid worsening of symptoms (vision loss, pain, photophobia, and conjunctival redness) over hours to days strongly suggests Pseudomonas infection and requires immediate referral to an ophthalmologist. A history of eye trauma while gardening is a risk factor for fungal keratitis, which also tends to be more common in the tropical regions.

Ophthalmologic examination – This includes an assessment of visual acuity, pupil size and reactivity, and any lesions or foreign bodies on the cornea. Fluorescein is used to evaluate for the presence of a corneal epithelial defect. The ophthalmologic evaluation of a red eye is discussed in further detail elsewhere. (See "The red eye: Evaluation and management", section on 'Ophthalmologic examination'.)

Slit lamp examination – If available, this should be performed to more carefully evaluate the cornea and other ocular structures (see 'Clinical features' above). This is also important to evaluate for a corneal perforation, which is an ophthalmologic emergency. Performance of slit lamp examination is discussed elsewhere. (See "Slit lamp examination", section on 'Procedure'.)

Diagnosis — The diagnosis of infectious keratitis is confirmed by slit lamp examination that demonstrates a corneal epithelial defect with an underlying stromal infiltrate, with or without hypopyon. Occasionally, infectious keratitis with large, fulminant ulcers may be visible without magnification.

Most contact lens-associated infectious keratitis is bacterial, but certain features suggest fungal or protozoal (eg, Acanthamoeba) pathogens. Ulcers caused by these organisms generally progress more slowly than bacterial infections. While both may occasionally manifest a ring-shaped stromal infiltrate, fungal infections typically have multiple satellite infiltrates with fluffy borders and occasionally a white plaque on the endothelial (inner) surface of the cornea (picture 10). Nonbacterial infections require special tests for diagnosis, as below.

Microbial culture — Obtaining corneal cultures is usually not necessary for initial treatment of small peripheral ulcers. However, cultures should be obtained if the infection is particularly severe (central infiltrate, large infiltrate >2 mm, associated with stromal melting, or multifocal), if it does not respond to initial empiric antibacterial therapy, if the patient has a history of corneal surgery, or if a nonbacterial infectious keratitis is suspected [66].

Cultures should be performed by an ophthalmologist. Specimens from the infected cornea may be obtained by scraping with a Kimura spatula (picture 11) or a disposable sterile scalpel blade. The peripheral borders of the infiltrate, often the leading edge of infection, may contain the most active organisms and therefore yield the most productive cultures. Swab cultures obtained with cotton-tipped applicators are often inadequate and are not recommended unless there is no other recourse. Commercially packaged quick culture kits consisting of a sterile swab and culture broth may also be used, with comparable results to traditional culture [67].

Specimens should be submitted for Gram stain and bacterial and fungal cultures; special media are required when nontuberculous mycobacterial or amoebic infections are suspected. Immunofluorescent stains may be helpful, but cultures are the top priority when there is limited sample.

Culture and Gram stain can be important in microbial identification of unusual bacteria, drug-resistant bacteria (eg, methicillin-resistant Staphylococcus aureus [MRSA]), or nonbacterial organisms such as fungi and Acanthamoeba. Chronic or atypical corneal infections may eventually require deeper lamellar corneal excisional biopsies for identification. Other specialized testing (eg, confocal microscopy or polymerase chain reaction assays) may be warranted for nonbacterial infections. Microbiologic diagnosis of fungal and Acanthamoeba keratitis are discussed elsewhere.

(See "Clinical manifestations and diagnosis of Fusarium infection", section on 'Diagnosis'.)

(See "Epidemiology, clinical manifestations, and diagnosis of Scedosporium and Lomentospora infections", section on 'Diagnostic techniques'.)

(See "Free-living amebas and Prototheca", section on 'Diagnosis'.)

Contact lenses, cases, and lens care systems may provide an alternative source for culture, especially when corneal cultures are negative or when antibiotic treatment has already been initiated, but they often harbor a wide spectrum of microorganisms, and culture results may be misleading or confusing [68-70].

Differential diagnosis — The presentation of typical symptoms and signs in a contact lens wearer make the diagnosis of infectious keratitis likely. Although sterile corneal ulcers can be seen in noninfectious keratitis, the distinction between infectious and noninfectious keratitis may be subtle or obscure and it is best to treat all ulcers as if they are infectious.

The general approach to evaluation of a patient presenting with a red eye and its main differential diagnoses are discussed in detail elsewhere. (See "The red eye: Evaluation and management".)

Initial management

General measures

All patients should be told to stop wearing contact lenses until further instruction.

Infected corneas should not be patched because the darkness, warmth, and humidity may be conducive to enhanced growth of microorganisms. Even clean-appearing contact lens-related corneal abrasions, without infiltrates, should not be patched because such abrasions may occasionally be early infections [21].

However, if the cornea is deeply ulcerated or perforated, a protective metal or plastic eye shield should be applied while awaiting ophthalmologic evaluation. (See 'Urgent ophthalmologic referral' below.)

Concurrent cycloplegic eye drops (eg, atropine, homatropine) may be used to reduce photophobia from ciliary spasm and to reduce the formation of pupillary adhesions to the lens (posterior synechiae).

Urgent ophthalmologic referral — All patients with suspected or confirmed infectious keratitis, regardless of severity, should be referred to ophthalmology urgently.

In addition to appropriate evaluation, treatment, and monitoring, ophthalmologic evaluation is important, as a delay in diagnosis and treatment may result in corneal perforation. Corneal perforation is a serious complication that may potentially lead to endophthalmitis and intraocular damage, which may warrant immediate surgical intervention (picture 12). In addition, severe infections may benefit from specialized treatments such as subconjunctival antibiotic injections or intrastromal injections [71] in addition to the eyedrop therapy.

In the event that ophthalmologic evaluation is not immediately available, the general clinician can cautiously proceed with initial antibiotic management, as below.

Initial antibiotic treatment — If urgent ophthalmology referral is not possible, appropriate antibiotic therapy should be started on initial presentation with ophthalmologic follow up in the next day or two. Empiric treatment with topical wide-spectrum antibiotic eye drops is an accepted community standard for contact lens keratitis [72,73]. We suggest empiric monotherapy with a topical fourth-generation fluoroquinolone (eg, besifloxacin, gatifloxacin, moxifloxacin) given hourly. An alternative treatment is alternating fortified cefazolin (50 mg/mL) (or fortified vancomycin [50 mg/mL] for patients allergic to penicillin or cephalosporins) with fortified gentamicin or tobramycin (14 mg/mL) eye drops every 30 minutes (eg, cefazolin or vancomycin given on the hour and the aminoglycoside given on the half hour) [73,74]. Earlier-generation fluoroquinolones (ofloxacin, levofloxacin, and ciprofloxacin) can be used if cost is an issue.

For most patients, hourly treatment is indicated for the first 24 to 48 hours. Drops are preferred because ointments have poor corneal bioavailability [75]. However, ointments may be used at bedtime to allow the patient to sleep through the night, but only after a positive response has been demonstrated to the initial intensive eyedrop treatment.

Fourth-generation fluoroquinolone therapy with moxifloxacin or gatifloxacin has been demonstrated to be equally effective to combination therapy of fortified cefazolin and tobramycin in one trial [76]. In a randomized trial of 61 patients evaluating these regimens, the overall rate of ulcer healing was 93 percent, and the time to healing was similar.

Antibiotic resistance is an emerging issue [77,78] and may be of particular concern with second- and third-generation fluoroquinolones [79]. Resistance even to fourth-generation fluoroquinolones has been described [80].

Avoid glucocorticoids — Concurrent glucocorticoid eye drops should absolutely be avoided in the acute phase of infectious keratitis because they can impede healing and mask signs of worsening infection.

However, after the infection is under good control, select patients with visually significant central corneal inflammation or a severe anterior segment inflammatory response may benefit from topical corticosteroids used together with the antimicrobial drugs. Such therapy can reduce inflammation and lessen visually significant central infiltrates [81] and may provide a better long-term clinical outcome [82]. However, glucocorticoid therapy should only be initiated by the ophthalmologist and only when the ulcer is responding well to antibiotic therapy.


Monitoring — The patient should be examined daily for the first three to five days until definitive improvement is noted, at which time the frequency of visits may be reduced as appropriate. The eye drop frequency may be cautiously reduced over days to weeks in correlation to the improvement, which can sometimes be slow.

Bacterial keratitis is expected to show signs of responding to appropriate antibiotic therapy within a week. In cases that fail to respond, nonbacterial keratitis or infection with resistant bacteria are possible reasons. (See 'Refractory cases' below.)

Duration of antibiotic therapy — Treatment should be continued for a minimum of two weeks and at least until the ulcer and other signs of infectious keratitis have fully resolved. Clinically visible healing may take weeks or, in rare instances, months. Some patients with more severe infections will require ongoing antibiotic treatment for several months. Healing is usually assessed by an ophthalmologist; drug effects on the cornea may delay or obscure clinical improvement, and so expert evaluation is warranted.

Refractory cases — Ulcers which fail to respond to therapy within a week should be seen by an ophthalmologist (ideally a cornea specialist) for obtaining cornea cultures and further diagnostic studies. In refractory cases, cultures may be invaluable in the identification and antibiotic sensitivities of the resistant organisms. (See 'Microbial culture' above.)

Additionally, corneal surgery may be indicated for extirpation of recalcitrant infectious foci, improvement of drug penetration, and to address corneal perforation. A conjunctival flap over the cornea may sometimes be required to arrest a persistent corneal ulcer but is not appropriate for fungal ulcers since organisms may survive under the flap.

Treatment of nonbacterial infectious keratitis, such as fungal or Acanthamoeba keratitis, is discussed elsewhere. (See "Treatment and prevention of Fusarium infection", section on 'Keratitis' and "Free-living amebas and Prototheca", section on 'Keratitis'.)

Resumption of contact lens wear — Several months after the infection has resolved (ie, the corneal ulcer has healed), resumption of contact lens wear is reasonable, but the patient should be cautioned on the risk of recurrence. Specifically, counseling about proper hygienic habits, contact lens care, avoidance of over-wear, and strict avoidance of overnight wear is essential. The risk of recurrence or adverse consequences of infection may be higher with coexisting ocular surface problems. For some patients, the ophthalmologist might suggest a type of lens other than the one worn prior to the infection or an alternative to contact lens wear altogether, such as spectacles or refractive surgery.

Prevention — Recommendations from the US Food and Drug Administration (FDA) for proper management of contact lenses to reduce infection risk are summarized in the table (table 1). These include using only multipurpose solution or one-step hydrogen peroxide-based solutions to care, clean, and store the lenses and, in addition, following contact lens case hygiene. Contact lens cases can become a repository and breeding ground for microorganisms. Daily rinsing and air-drying the case, alcohol swabbing, and quarterly case replacement are recommended to reduce the growth and attachment of microbial flora. A more complete discussion of contact lens care is available separately. (See "Overview of contact lenses", section on 'Lens care and use'.)

In addition, the US Centers for Disease Control and Prevention (CDC) 2015 recommendations include the following guidelines to avoid contact lens-related infections [1]:

Never sleep in contact lenses

Avoid exposing lenses to water (avoid showering or swimming in contact lenses)

Replace contact lens as often as recommended by eye care provider

Replace contact lens case at least once every three months

If experiencing eye pain, redness, or blurry vision, remove contact lens and seek evaluation by an eye care provider

Prognosis — For most patients who receive timely and appropriate treatment, the infection can be cleared and most symptoms (ie, redness, irritation, photophobia, pain) resolved. However, depending on the location and severity of the ulcer, a corneal scar can result and the visual consequences can be variable, ranging from inconsequential to visually disabling. If appropriate treatment is delayed, infectious keratitis may lead to serious, blinding complications including corneal scarring (leukoma), vascularization (picture 13), perforation, and irregular astigmatism. Intraocular complications may include cataract, glaucoma, endophthalmitis, and phthisis bulbi (endstage blind eye with low intraocular pressure, often resulting in shrinkage of the globe), which may necessitate enucleation of the eyeball.


Noninfectious complications of contact lens wear are minimized with a well-fitted lens that rests on the tear film and moves only enough to allow good fluid and gas exchange. (See 'Noninfectious complications' above.)

Sterile corneal infiltrates are collections of inflammatory cells that appear as white lesions in the anterior stroma. They are usually asymptomatic and respond to topical corticosteroids and eye hygiene measures. (See 'Sterile corneal infiltrates' above.)

Corneal epithelial problems are diagnosed by fluorescein dye staining. Punctate staining is common and is caused by a number of mild insults related to contact lens wear; larger defects can be due to mechanical trauma. Corneal abrasions should be treated with topical antibiotics with pseudomonal coverage and removal of the contact lens. We recommend not patching the eye for small corneal abrasions (Grade 1A). (See 'Corneal epithelial problems' above.)

Other noninfectious contact lens-related complications may result from hypoxic, toxic, or immune reactions, a poorly fit tight contact lens, or a dislocated lens. (See 'Noninfectious complications' above.)

Contact lens wear increases the risk of infectious keratitis, with increased risk in extended-wear lenses and in users with poor technique for contact lens preparation or disinfection. Patients typically present with a painful red eye; the diagnosis is confirmed by slit lamp examination that demonstrates a corneal epithelial defect with an underlying stromal infiltrate, with or without hypopyon. Cases are typically bacterial, and treatment is usually empiric for peripheral small ulcers. Microbial culture, involving corneal scraping, is indicated for patients with suspected severe infectious keratitis and for those who do not respond to empiric antibiotic treatment. (See 'Infectious keratitis' above.)

Patients with suspected infectious keratitis related to contact lens wear should be promptly referred to an ophthalmologist. If immediate referral is not possible, empiric topical antibiotics can be initiated. We suggest a fourth-generation fluoroquinolone (besifloxacin, gatifloxacin, or moxifloxacin) (Grade 2B). Alternatively, alternating therapy with a fortified aminoglycoside and fortified cephalosporin (or vancomycin) is an acceptable choice. Patients should have close follow-up at 24 hours. The use of glucocorticoids and patching should be strictly avoided. (See 'Initial management' above.)

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