Contact lens-related peripheral ulcer (CLPU) is a non-infectious corneal inflammation that appears as a single small infiltrate in the peripheral cornea in association with contact lens (CL) wear. Internationally it is also called “contact lens-induced peripheral ulcer,” and in Japan it is described as “peripheral corneal infiltrate.” The pathological entity is localized neutrophil infiltration, positioned as an immune/inflammatory reaction without infection. The name ulcer derives from historical nomenclature, but because it does not necessarily involve an epithelial defect and its course is relatively favorable, whether it should be called an infiltrate or an ulcer is a condition debated internationally.
CLPU is positioned as one of the group of CL-related non-infectious corneal infiltrative lesions called Corneal Infiltrative Events (CIE)4). CIE includes, in addition to CLPU, contact lens-induced acute red eye (CLARE), non-central infiltrative keratitis (IK), and asymptomatic infiltrates (AI). These form a continuous spectrum, and clinically the core challenge in practice is differentiation from microbial keratitis.
CL wear is the largest risk factor for microbial keratitis in the United States1), and in the epidemiological study by Stapleton et al., the annual incidence of all corneal infiltrative events in CL wearers was reported to be approximately 3–6 per 100 person-years6). Among these, CLPU accounts for a certain proportion as small, well-demarcated infiltrates, and is characterized by being more frequent than microbial keratitis but following a milder course. In the United States, approximately 71,000 cases of microbial keratitis are estimated to occur annually, and CL wearers form a large population within this1).
CLPU has not been completely suppressed even after the widespread adoption of modern silicone hydrogel lenses7). While highly oxygen-permeable materials have reduced hypoxia-related complications, extended wearing time, poor care, and lens case contamination remain, so it must be recognized as a representative non-infectious inflammatory event encountered in CL wearers. In the multicenter cohort study by Sweeney et al., the clinical features of CIE including CLPU were described in detail, and the lesion diameter, location, and anterior chamber inflammation pattern of CLPU were shown to be important points for differentiating it from microbial keratitis5).
QWhat is the difference between CLPU and microbial keratitis?
A
CLPU is a non-infectious corneal infiltrate caused by the host immune response to bacterial cell components adhering to contact lenses, and appears as a single small lesion approximately 1–2 mm in diameter in the peripheral cornea. It is not accompanied by anterior chamber inflammation, epithelial defects are also minor, the epithelium repairs in 4–5 days, and it resolves in 1–2 weeks. On the other hand, microbial keratitis is an infection caused by pathogens invading and proliferating in the corneal stroma; the lesion is larger, accompanied by irregularly bordered epithelial defects, anterior chamber inflammation or hypopyon, and severe pain, and delayed treatment leads directly to corneal perforation or blindness. If any of the following is present—infiltrate diameter greater than 2 mm, less than 3 mm from the visual axis, or worsening within 48 hours—microbial keratitis should be strongly suspected, and it is necessary to switch to corneal scraping culture and intensive antimicrobial treatment1).
The subjective symptoms of CLPU are relatively mild to moderate and develop acutely. Representative symptoms are as follows.
Foreign body sensation/discomfort: The most frequent initial symptom. It often appears in only one eye.
Eye pain: Often mild to moderate, but relatively severe pain is reported when accompanied by an epithelial defect or when an upper lesion causes friction with blinking.
Conjunctival hyperemia: Characterized by localized ciliary injection adjacent to the lesion site.
Tearing/blurred vision: Depending on the lesion location, transient visual decrease may be noticed.
Asymptomatic: There are also asymptomatic cases discovered incidentally during routine examination.
When subjective symptoms are severe, or when all three signs of conjunctival hyperemia, mucopurulent ocular discharge, and severe pain occur together, microbial keratitis is possible, and it is necessary to proceed with a workup based on the premise of infection rather than adhering to a diagnosis of CLPU1). In addition, it should be noted that all CLs reduce corneal sensation (hypoesthesia), so some cases do not report symptoms until the condition has become severe.
The clinical appearance of CLPU is relatively uniform, observed as small peripheral corneal infiltrates with clear borders.
Location: Peripheral cornea, approximately 1-2 mm inside the limbus. It occurs most often superiorly, but can also occur inferiorly, temporally, or nasally.
Shape: Oval or round, rarely irregular. The borders are relatively distinct.
Size: Typically about 1-2 mm in diameter, and exceeding 4 mm is rare5).
Depth: Limited to the corneal epithelium through the superficial stroma (anterior one-third), with no progression to deeper layers.
Epithelial defect: Often mildly present, but sometimes absent. Even when present, the border between the lesion and the epithelial defect is regular.
Anterior chamber inflammation: Usually not observed. Even if mild cells are present, it does not lead to hypopyon.
Conjunctival hyperemia: Shows ciliary injection localized near the lesion. A characteristic feature is that it is not circumferential.
Single lesion: Multiple lesions are rare, and most are a single lesion.
With fluorescein staining, only the epithelial defect at the center of the infiltrate stains faintly. The fact that it stains mildly directly over the lesion while the entire infiltrate does not stain helps distinguish it macroscopically from infectious ulcers. Scarring may occur during the course, leaving a punctate round opacity (nummular scar), but because it is peripheral, the impact on visual function is usually minor4).
Comparison of clinical findings between CLPU and microbial keratitis
In the management of CLPU, differentiation from microbial keratitis is the most important consideration. The clinical features of both are compared below.
CLPU is a condition with a favorable course, and if contact lens use is discontinued and appropriate eye drop treatment is given, repair of the corneal epithelium is usually completed in 3–5 days. After that, it generally takes 1–2 weeks for the infiltrative lesion and conjunctival hyperemia to resolve. After healing, a punctate corneal opacity (nummular scar) may remain, but because the lesion is located in the peripheral cornea, the effect on visual acuity is usually minor. However, if there is no improvement after 2 weeks, or if the condition worsens after treatment is started, there is a possibility of progression to microbial keratitis or misdiagnosis, and reevaluation is always necessary.
Although CLPU is not infectious, it develops through a combination of multiple factors associated with CL wear. The main risk factors can be broadly organized into two groups: “CL wear and care-related factors” and “microbiological factors.”
CL Wear and Care-Related Factors
Sleeping in lenses/continuous wear: Sleeping while wearing CLs is the greatest risk for microbial keratitis and is also a major risk factor for inflammatory events including CLPU1,7). In a case-control study by Carnt et al., sleeping in lenses was reported to be a modifiable risk factor that increases AK risk by approximately 4-fold (OR 3.93) even among daily disposable lens users11).
Lens case contamination and biofilm: If the case is not replaced for 3 months or longer, or if the case is not dried inside, biofilm forms and becomes a reservoir for Gram-negative bacteria and Staphylococcus aureus9).
Care product incompatibility and omission of rubbing: When multipurpose solution (MPS) is used alone and “rubbing” is omitted, bacterial deposition on the lens increases markedly4).
Lens Type and Usage Status
Conventional/frequent replacement SCLs: Two-week frequent replacement SCLs (FRSCLs) and monthly conventional SCLs are more likely to involve poor care and are frequently associated with both CLPU and CLARE.
Silicone hydrogel lenses: Although high oxygen permeability has reduced hypoxic complications, the incidence of CIE is still not negligible7). Mechanical irritation caused by the hardness of the material is added as another factor.
Foreign bodies under the lens: If makeup particles or dust remain under the lens during sleep, the foreign bodies are pressed into the cornea and become a starting point for epithelial damage and immune reactions.
Microbiological Factors
Staphylococcus aureus adhesion to lenses: Staphylococcus aureus is often detected from lenses, lens cases, and the ocular surface at CLPU onset, and cell wall components of this bacterium are thought to be the main antigens in the immune response10).
Gram-negative bacterial endotoxin: Lipopolysaccharide (LPS) produced in lens cases by Pseudomonas aeruginosa, Serratia, Enterobacter, and others can also induce inflammatory reactions.
Overgrowth of commensal bacteria: The amount of commensal bacteria on the eyelid margin and in tears changes with CL wear, and in some cases this leads to overgrowth of specific bacterial species8).
In the prospective cohort of Stapleton et al., continuous wear of silicone hydrogel lenses (30 days) reached an annual incidence of CIE of approximately 20 cases per 100 person-years, reported to carry a significantly higher risk than daily disposable lenses6,7). In Japan, CL wear accounts for the largest proportion of triggers for infectious keratitis, showing a bimodal peak in people aged 20-29 and 60-69, but the majority of those aged 20-29 are CL wear-related3). Younger CL-wearing generations are likely to frequently encounter mild CIE such as asymptomatic infiltrates and CLPU.
One-day disposable (DD) lenses reduce the risk of Acanthamoeba keratitis by approximately 3.84-fold compared with DW reusable lenses, and switching to DD is estimated to prevent 30-62% of severe corneal inflammation cases11). For inflammatory events in general, including CLPU, switching to DD lenses is a reasonable preventive strategy that can eliminate the risk of poor care.
QAre one-day lenses safe?
A
One-day disposable soft contact lenses do not require the use of a lens case, greatly reducing the risk of infection and inflammation from biofilms and contaminated solution. The frequency of CLPU due to protein deposits or incompatibility with care solutions is also reported to be lower than with frequent replacement or conventional lenses7,8). The risk of Acanthamoeba keratitis is also reduced by approximately 3.84-fold compared with DW reusable lenses, and a public health preventive effect can be expected11). However, even with one-day lenses, CLPU and microbial keratitis can occur if usage rules are violated, such as sleeping while wearing lenses, extended wear, or excessively long wear, so adhering to wearing time and immediately discontinuing use when abnormalities occur are fundamental.
The diagnosis of CLPU is based on clinical findings. Special tests are not required, but a systematic evaluation to reliably exclude microbial keratitis is essential.
In CLPU care, systematically taking a history of CL wearing status and care habits is key to differential diagnosis and risk assessment. The minimum items to confirm are as follows.
Type of CL and wearing history: soft/hard/color CL, one-day/2-week frequent replacement/monthly, presence or absence of silicone hydrogel, time of starting use
Wearing time and wearing pattern: daily wearing time; presence or absence of overnight wear, continuous wear, or extended wear
Care habits: frequency of lens case replacement and drying habits, whether rubbing and rinsing is performed, type of care solution (MPS/hydrogen peroxide-based/povidone-iodine), reuse of storage solution
Onset and course of symptoms: time of onset, whether acute or gradual onset, presence or absence of worsening within 48 hours, diurnal variation of symptoms
Details of subjective symptoms: degree of pain (mild to moderate or severe), nature of eye discharge (mucoid/purulent), presence or absence of photophobia and lacrimation
Episodes immediately before onset: foreign body entering under the lens, forced wearing or removal, wearing during bathing or swimming, contact with makeup
Medical history: past similar episodes, history of CL-related keratitis, comorbid conditions such as atopic dermatitis or dry eye
CL replacement schedule: adherence to the replacement schedule
Situation during the 24–48 hours before onset: awareness of foreign body sensation or foreign body under the lens
Slit-lamp microscopy is central to diagnosis. When observing keratitis, a procedure that evaluates the lesion in the following 5 steps is useful.
Diffuser light: grasping the extent of opacity across the entire cornea
Retroillumination: observation of the depth of cellular infiltration in the infiltrative lesion and anterior chamber inflammation (especially keratic precipitates)
Wide slit beam: observation of the entire corneal surface
Narrow slit beam: confirmation of lesion depth and anterior chamber inflammation
Fluorescein staining: evaluation of epithelial damage and the state of the tear film
CLPU is characterized by a single small infiltrate in the peripheral cornea and no inflammatory cells in the anterior chamber. In eyes wearing HCLs, observing lens surface deposits and wettability before fluorescein staining may provide diagnostic clues.
This is essential for determining the pattern of epithelial defect. In CLPU, only a localized epithelial defect at the center of the infiltrate may stain, or there may be no staining at all. The following are assessed based on the staining site and morphology.
Presence or absence of punctate staining directly over the lesion
Presence or absence of extensive surrounding epithelial damage (if extensive, suspect microbial etiology)
Coexistence of other CL-related epithelial disorders such as 3 and 9 o’clock staining, smile mark SPK, or SEAL
If any of the following are present, it is necessary to manage the case as microbial keratitis rather than CLPU1).
Infiltrate larger than 2 mm in diameter
Location less than 3 mm from the visual axis
Worsening of the clinical course 48 hours after starting treatment
Anterior chamber inflammation or hypopyon
Severe pain and circumferential conjunctival hyperemia
Infiltrate with an irregular epithelial defect
If these danger signs are present, or if there is no tendency toward improvement within 48 to 72 hours after diagnosing CLPU, Gram staining, culture, and susceptibility testing of corneal scrapings should be performed, and treatment should be switched to fortified antimicrobial therapy. The third edition of the Japanese guidelines for the management of infectious keratitis strongly recommends specimen collection and culture testing before administering antimicrobials when CL-related keratitis is suspected to be severe or refractory3). Acanthamoeba keratitis (AK) is a serious corneal infection in CL wearers, and the majority of AK patients (88% or more) are CL wearers. In differentiating from CLPU, confirm that the pain is severe and worsens at night, the presence of radial keratoneuritis (early sign), and poor response to treatment.
Understanding non-infectious corneal lesions that resemble CLPU is helpful for differential diagnosis.
Marginal keratitis (catarrhal corneal infiltrate): A type III/IV allergic reaction to Staphylococcus aureus at the eyelid margin. It presents as an elongated infiltrate parallel to the limbus, separated by a clear zone.
Corneal phlyctenule: A nodular lesion with vascular invasion, representing a delayed-type hypersensitivity reaction to tuberculosis or sebaceous gland inflammation.
Superior epithelial arcuate lesion (SEAL): Arcuate epithelial damage caused by mechanical irritation above the SCL. Infiltration is mild, and it is distinguished by the fluorescein staining pattern.
Thygeson punctate superficial keratitis: Recurrent and bilateral multiple stellate infiltrates. Its association with CL wear is weak.
3 and 9 o’clock staining: Localized staining near the limbus caused by HCL wear. Infiltration is usually absent.
Microbial keratitis: As mentioned above, differentiate by whether it is progressive, more centrally located, and whether there is anterior chamber inflammation.
The treatment of CLPU rests on four pillars: (1) immediate discontinuation of CL wear, (2) broad-spectrum antibacterial eye drops, (3) concomitant use of low-concentration steroids after infection is ruled out, and (4) promotion of epithelial repair. Many cases heal within about 1 week with eye drop treatment, and pharmacotherapy is the mainstay of treatment.
The Four Pillars of Treatment
Immediate discontinuation of CL: This is the most fundamental principle of treatment. Do not resume wear until resolution of the infiltrate, disappearance of conjunctival hyperemia, and epithelial repair have been confirmed.
Broad-spectrum antibacterial eye drops: Until differentiation from infection is complete, broad-spectrum antibiotic eye drops are used first. Fluoroquinolones (0.5% levofloxacin, 0.5% moxifloxacin, 1.5% high-concentration levofloxacin formulation, etc.) are used 4 to 6 times daily.
Low-concentration steroid eye drops: Once the possibility of infection has been excluded, 0.1% fluorometholone ophthalmic solution is used 4 times daily for 2 to 4 weeks. Suppressing inflammation leads to faster symptom improvement and is expected to reduce scar formation. In severe cases, consider increasing the dose or systemic administration.
Support for epithelial repair: Use 0.1% or 0.3% sodium hyaluronate ophthalmic solution 4 to 6 times daily to promote epithelial repair and stabilize the tear film.
Treatment Duration and Follow-up
3–5 days after the initial visit: Confirm epithelial repair. Infiltrates may persist, but evaluate whether they show a tendency to shrink.
1 week after the initial visit: Confirm resolution of conjunctival hyperemia and reduction of the infiltrate. If symptoms are absent, taper the antibacterial eye drops.
2 weeks after the initial visit: The infiltrate has mostly resolved. If residual punctate opacities are in the peripheral area, their impact on visual function is minimal.
Recurrence prevention: When resuming CL wear, always identify the causative factors (poor care, contaminated case, excessive wearing time, sleeping while wearing lenses), and resume only after confirming improvement. Actively consider switching to daily disposable lenses or to highly oxygen-permeable SiHy lenses. Reviewing the wearing schedule (no continuous wear) and ensuring thorough care methods (rubbing and disinfection) are also essential.
Concomitant use of low-concentration steroids for CLPU is considered effective for prompt resolution of the infiltrate and reduction of scarring, and is a recommended treatment. However, caution is required when using them at a stage when infection cannot be completely ruled out. In the third edition of the Japanese guidelines for the management of infectious keratitis, concomitant steroid eye drops for bacterial keratitis are “weakly recommended against,” and easy use before identification of the causative organism should be judged cautiously3). In particular, steroid use for Acanthamoeba, fungi, and Nocardia poses a clear risk of worsening the condition and is contraindicated1,3).
In actual clinical practice, for typical CLPU meeting the five conditions of ① single, small, peripheral, ② no epithelial defect to mild, ③ no anterior chamber inflammation, ④ mild pain, and ⑤ localized conjunctival hyperemia, fluorometholone is used concomitantly; on the other hand, when the decision is difficult, a conservative approach of antibiotic monotherapy plus NSAID eye drops (such as bromfenac) while observing the course is safe.
When the diagnosis of CLPU is not established and microbial keratitis is highly likely, follow the flow below based on the AAO Bacterial Keratitis PPP1).
No vision threat (infiltrate 2 mm or less and non-central ulcer at least 3 mm away from the visual axis): Perform empirical treatment with fluoroquinolone eye drops and assess for improvement at 48 hours.
Vision threat present (infiltrate over 2 mm, less than 3 mm from the visual axis, or worsening 48 hours after starting treatment): Perform Gram staining and culture by corneal scraping, and start fortified antibacterials such as vancomycin 50 mg/mL plus fortified tobramycin 14 mg/mL every hour. Change drugs according to culture results.
Combination of fortified aminoglycosides (tobramycin 14 mg/mL, gentamicin 14 mg/mL) and vancomycin (25–50 mg/mL) is a standard regimen covering both Gram-positive cocci and Gram-negative bacilli1). When Acanthamoeba is suspected, multidrug combination therapy with polyhexamethylene biguanide, propamidine isethionate, neomycin, etc. is selected.
Relationship with Therapeutic Contact Lenses (BCL)
In patients wearing therapeutic contact lenses (bandage contact lenses, BCL) for other conditions such as recurrent corneal erosion or bullous keratopathy, sterile infiltrates resembling CLPU may develop. In the AAO Corneal Edema and Opacification PPP, thin lenses with high water content and high Dk value are considered safe when using BCL, and concomitant use of prophylactic broad-spectrum antibiotics is recommended to prevent secondary infection2). BCL is a temporary means of pain relief and promotion of epithelial repair, and does not serve as a long-term solution for corneal edema2). If CLPU is suspected during BCL wear, temporarily remove the BCL, directly evaluate the lesion, and make a judgment in parallel with antibiotic treatment.
QCan I resume wearing contact lenses during treatment?
A
During treatment of CLPU, contact lens wear must be completely discontinued. The criteria for resuming are after it has been confirmed that: ① the corneal infiltrate has completely resolved, ② conjunctival hyperemia has disappeared, ③ the epithelial surface has completely healed, ④ there are no subjective symptoms, and ⑤ the causative factors (poor care, contaminated lens case, excessive wearing time, sleeping while wearing lenses, etc.) have been identified and corrected. In many cases, this takes 2–3 weeks or more from the start of treatment. When resuming, switching to a daily disposable type or changing to silicone hydrogel lenses is recommended. Replace the lens case every month, rub-clean the lenses thoroughly, and dry the lens case.
The pathophysiology of CLPU is understood as the host’s innate immune response to microbial components adhering to the contact lens surface. It is characterized by being not an infection but sterile inflammation due to interaction with bacterial components.
In eyes wearing lenses, tear exchange is restricted, and mucin, proteins, and lipids in the tears deposit on the lens surface, forming a biofilm-like film. Commensal bacteria from the eyelid margin and tears, especially Staphylococcus aureus, readily colonize this film10). Peptidoglycan and lipoteichoic acid, which are cell wall components produced by Staphylococcus aureus, and endotoxin (lipopolysaccharide, LPS: derived from gram-negative bacteria) activate the innate immune system via Toll-like receptors (TLR2, TLR4) expressed on corneal epithelial cells.
Activated corneal epithelium releases inflammatory cytokines and chemokines such as IL-1β, IL-6, IL-8, and CXCL1, causing neutrophils derived from peripheral blood to migrate and infiltrate the peripheral corneal stroma4). This neutrophil-predominant inflammatory response forms the clinical picture of a “single, well-demarcated small infiltrate.” In fact, while Staphylococcus aureus is often isolated from the lens or conjunctival sac at CLPU onset, corneal scrapings are often sterile, supporting that this is an antigen response rather than an infection10). It can be positioned as a type III or type IV immune reaction to proteins or bacteria adhering to the CL, and immune cell infiltration from limbal vessels contributes to lesion formation.
Synergistic effects of mechanical and hypoxic factors
CL wear imposes continuous mechanical friction and hypoxic stress on the corneal surface, altering epithelial barrier function and innate immune thresholds4). Mechanical stimulation is strong at sites where the upper eyelid contacts the upper edge of the lens with each blink, consistent with the finding that CLPU frequently occurs in the superior peripheral cornea. Silicone hydrogel lenses add mechanical stimulation due to the hardness of the material, and lens edge indentation or concurrent SEALs may be observed7).
Hypoxia activates the hypoxia-inducible factor (HIF) pathway, increases expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases, and promotes neovascularization and stromal remodeling. Chronic hypoxia and repeated inflammation may also be involved in long-term impairment of the limbal stem cell niche and neovascular invasion.
CLPU forms part of the spectrum of sterile inflammatory diseases as a subset of Corneal Infiltrative Events4,8).
CLPU: Well-demarcated single small infiltrate, mostly superior to peripheral, mild epithelial defect, with a distinct clinical picture.
CLARE (Contact Lens-induced Acute Red Eye): Causes acute conjunctival hyperemia and multiple non-central infiltrates after overnight wear. The endotoxin hypothesis is prominent, and an association with lens case contamination has been reported.
Infiltrative Keratitis (IK): A condition with moderate symptoms and multiple non-central infiltrates; symptoms are stronger than CLPU but milder than CLARE.
Asymptomatic Infiltrative Keratitis (AIK): Multiple infiltrates with minor symptoms.
These are distinguished by differences in clinical presentation and course, but they share the same underlying pathophysiology (a sterile inflammatory response to bacterial components)8). The decisive difference between CLPU and microbial keratitis is that the former is a host immune response, whereas in the latter the pathogen proliferates in the corneal stroma. Therefore, clinical judgment requires a comprehensive assessment of whether improvement is obtained with empiric antibiotic administration, the presence or absence of anterior chamber inflammation, the rate of infiltration progression, and the results of culture testing.
The lens case plays an important role as a microbial reservoir in CLPU and in CIE in general9). In a review by Wu et al., bacterial contamination was found in 30-80% of lens cases in use, and the most frequently contaminating organisms reported were Staphylococcus aureus, Pseudomonas aeruginosa, and Serratia9). Bacteria within biofilms have high resistance to disinfectants, and complete eradication with MPS alone is difficult, so rubbing and cleaning, along with regular replacement and drying of the case, are essential.
Basic and clinical research on CL-related corneal infiltrative events has continued to advance in recent years. The TFOS CLEAR (Contact Lens Evidence-Based Academic Reports) published in 2021 systematized the classification, epidemiology, risk factors, and preventive measures of CIE, and has become an international standard reference for inflammatory complications including CLPU4). TFOS CLEAR emphasizes that CIE remains an important safety issue in CL wear, and that risk stratification based on the combination of lens material, wearing schedule, and care products is important.
As predictive biomarkers, profiles of inflammatory cytokines in tears (IL-6, IL-8, MMP-9), microbiome analysis of the conjunctival surface, and TLR expression patterns are being investigated, but they are not yet at the stage of clinical application. Antimicrobial modification of lens materials (silver ion incorporation, peptide surface modification) is also undergoing verification from the standpoints of both long-term safety and clinical efficacy.
Epidemiological background and public health significance of CLPU
With the increase in CL wearers, the number of cases of non-infectious corneal infiltrates, including CLPU, is also increasing. In the Australian cohort of Stapleton et al., the annual incidence of infectious keratitis in CL wearers was 2-4 cases per 10,000 person-years6), and non-infectious infiltrates occur even more frequently. CL wearers worldwide number approximately 300 million12), and improving CL safety from a public health standpoint is an important issue.
Switching to DD lenses not only reduces the risk of AK by approximately 3.84-fold11), but is also thought to reduce the risk of inflammatory events in general, including CLPU. TFOS DEWS III clearly states that CL wear is a trigger for dry eye and ocular surface disorders13), and proactive management of dry eye is also important in the prevention of CLPU.
The TFOS Lifestyle Report analyzes in detail the relationship between modern lifestyles and CL-related complications14), and points out that when long hours of digital device use, VDT work, and irregular sleep overlap, CL safety is markedly reduced. In the prevention of CLPU as well, reviewing lifestyle habits can be an effective intervention.
Stapleton F, Bakkar M, Carnt N, Chalmers R, Vijay AK, Marasini S, et al. CLEAR - Contact lens complications. Contact lens & anterior eye : the journal of the British Contact Lens Association. 2021;44(2):330-367. doi:10.1016/j.clae.2021.02.010. PMID:33775382.
Sweeney DF, Jalbert I, Covey M, Sankaridurg PR, Vajdic C, Holden BA, et al. Clinical characterization of corneal infiltrative events observed with soft contact lens wear. Cornea. 2003;22(5):435-42. doi:10.1097/00003226-200307000-00009. PMID:12827049.
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Loretta Szczotka‐Flynn, Mireya Diaz. Risk of Corneal Inflammatory Events with Silicone Hydrogel and Low Dk Hydrogel Extended Contact Lens Wear: A Meta‐Analysis. OVS. 2007;84(4):247-256. doi:10.1097/opx.0b013e3180421c47.
Steele KR, Szczotka-Flynn L. Epidemiology of contact lens-induced infiltrates: an updated review. Clinical & experimental optometry. 2017;100(5):473-481. doi:10.1111/cxo.12598. PMID:28868803.
Wu YT, Willcox M, Zhu H, Stapleton F. Contact lens hygiene compliance and lens case contamination: A review. Contact lens & anterior eye : the journal of the British Contact Lens Association. 2015;38(5):307-16. doi:10.1016/j.clae.2015.04.007. PMID:25980811.
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. 2000;19(1):116-20. doi:10.1097/00003226-200001000-00023. PMID:10632021.
Carnt N, Minassian DC, Dart JKG. Acanthamoeba Keratitis Risk Factors for Daily Wear Contact Lens Users: A Case-Control Study. Ophthalmology. 2023;130(1):48-55. doi:10.1016/j.ophtha.2022.08.002. PMID:35952937.
Craig JP, Alves M, Wolffsohn JS, Downie LE, Efron N, Galor A, et al. TFOS Lifestyle Report Executive Summary: A Lifestyle Epidemic - Ocular Surface Disease. The ocular surface. 2023;30:240-253. doi:10.1016/j.jtos.2023.08.009. PMID:37659474.
Jones L, Craig JP, Markoulli M, Karpecki P, Akpek EK, Basu S, et al. TFOS DEWS III: Management and Therapy. American journal of ophthalmology. 2025;279:289-386. doi:10.1016/j.ajo.2025.05.039. PMID:40467022.
Wolffsohn JS, Lingham G, Downie LE, et al. TFOS Lifestyle: Impact of the digital environment on the ocular surface. Ocul Surf. 2023;28:213-252. doi:10.1016/j.jtos.2023.04.004.
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