Contact lens (CL) complications are a general term for corneal and conjunctival disorders caused or triggered by CL wear. The severity ranges from asymptomatic minor findings to severe cases such as corneal ulcers.
The main mechanisms by which CLs induce ocular disorders can be broadly classified into the following five categories.
In the examination of CL complications, it is important to infer the cause from corneal findings and eliminate that cause. Explain the cause, healing period, presence of sequelae, and necessity of CL change individually, and provide appropriate treatment.
The main subjective symptoms of CL complications are as follows.
Particular caution is required when hyperemia, discharge, and pain occur together, as this may indicate corneal infection.
All CLs reduce corneal sensitivity (hypoesthesia). Due to this reduced sensitivity, CL wearers may have difficulty noticing early symptoms of corneal damage.
Classifying fluorescein staining patterns by extent (punctate, patchy, linear) and depth (SPK, corneal erosion, corneal ulcer) helps identify the cause.
3-and-9 o'clock staining (HCL)
Location: Limited to the 3 and 9 o’clock positions at the corneal limbus
Cause: During blinking, the HCL moves approximately 2 mm vertically, causing localized dryness as tears are drawn in from the 3 and 9 o’clock directions
Course: Mild cases heal in 3–5 days. Progression to erosion requires about 1 week and may leave corneal opacity
Smile-mark superficial punctate keratopathy (SCL)
Location: Lower pupillary area (corresponding to the shape of a smiling mouth)
Cause: Occurs in patients with pre-existing dry eye due to reduced tear fluid under the lens
Course: Managed with dry-eye eye drops. Advise early removal from the evening onward
Diffuse superficial punctate keratopathy (HCL/SCL)
Location: Nearly uniform across the entire cornea
Cause: Oxygen deficiency due to CL wear. Lens deposits add mechanical irritation and worsen the condition
Course: Heals in 4–5 days with CL discontinuation and eye drops
Other punctate lesion patterns are as follows.
| Pattern | Cause | Features |
|---|---|---|
| Donut-shaped superficial punctate keratitis | Color CL pigment exposure / SiHy + PHMB | Sparse in the center, concentrated peripherally |
| Big-mouth superficial punctate keratitis | Oxygen deficiency with prism-ballasted SCL | Localized to the lower two-thirds of the cornea |
| Ring-shaped staining | SiHy and care product incompatibility | Sharp decline since 2010 |
First, remove the CL immediately. If pain is mild and there is no vision loss, you may discontinue wear and observe until the next day. However, if accompanied by redness, discharge, or severe pain, infectious keratitis is possible, so promptly visit an ophthalmologist. Do not discard the removed CL—bring it to your appointment to help identify the cause.
Contact lens wear is one of the greatest risk factors for microbial keratitis. Causative organisms include Pseudomonas aeruginosa, Staphylococcus, Streptococcus, and Serratia. It has been reported that 88% of patients with Acanthamoeba keratitis (AK) were contact lens wearers.
Daily disposable lenses require no lens care, eliminating the risk of case contamination and minimizing protein buildup, making giant papillary conjunctivitis and care-solution-related complications unlikely. However, dry-eye-related smile-mark punctate keratopathy and complications from overnight wear can still occur with daily disposable lenses.
Slit-lamp microscopy is essential for diagnosing CL-related corneal disorders. In HCL wearers, a key point is to observe the lens surface for deposits and wettability before staining with fluorescein. Deposits become visible as the lens surface dries.
Useful for determining patterns of epithelial defects. The cause can be inferred from the location, morphology, and extent of staining.
Acute epithelial edema can be misdiagnosed as a full-thickness epithelial defect. Even without epithelial defects, tight junctions can weaken and allow fluorescein penetration, causing the entire cornea to appear stained 10 minutes after application.
| Differential Diagnosis | Key Differentiating Features |
|---|---|
| Superior Limbic Keratoconjunctivitis | Conjunctival epithelium also stains |
| Infectious Corneal Ulcer | Confirmed by culture test |
| Corneal Herpes | Dendritic ulcer. Pseudodendritic is CL-related |
In the differential diagnosis between SEALs and superior limbic keratoconjunctivitis (SLK), SLK differs in that the conjunctival epithelium also stains with fluorescein. Pseudodendritic keratitis is seen with HCL binding and resembles the dendritic ulcer of herpes keratitis in that the ends of linear lesions branch into two or more branches.
Discontinuation of CL wear and removal of the cause are the basics. Based on the corneal findings, the cause is inferred, and the healing period, presence or absence of sequelae, and necessity of CL change are explained individually.
After healing, CL change according to the cause is performed. Changing to SCL for 3-and-9 o’clock staining, selecting a safe SCL for SEALs, and changing to a silicone hydrogel lens with excellent water retention for smile-mark superficial punctate keratopathy are effective.
Treatment consists of discontinuing CL wear and using antibiotic + low-concentration steroid (0.1% fluorometholone) eye drops. Steroid use is desirable because infiltrative lesions may remain as opacity, but if poor compliance is anticipated, NSAID eye drops are used to monitor the course.
No Visual Threat
Indications: Small non-central ulcer with infiltration ≤2 mm and ≥3 mm from the visual axis
Treatment: Empiric therapy with fluoroquinolone eye drops
Visual Threat
Indications: Infiltration >2 mm, <3 mm from the visual axis, or worsening after 48 hours of treatment
Treatment: Perform corneal culture + Gram stain, initiate vancomycin + fortified tobramycin eye drops every hour. Adjust medication based on culture results.
Immediate discontinuation of contact lenses is mandatory. Common causative organisms include Pseudomonas aeruginosa and Staphylococcus species. For Acanthamoeba keratitis, combination therapy with polyhexamethylene biguanide, propamidine isethionate, and other agents is used.
The mainstay is discontinuation of contact lens use or switching to daily disposables. Use 0.1% fluorometholone 4 times daily for 1–2 weeks. Even after symptom improvement, returning to the original lens often leads to recurrence; changing the lens type is recommended.
When using BCL for pain relief in microcystic and bullous corneal epitheliopathy, thin lenses with high water content and high Dk value are considered safe2). Concomitant use of prophylactic broad-spectrum antibiotics is recommended to prevent secondary infection2). BCL does not provide a long-term solution for corneal edema2).
Silicone hydrogel lenses have dramatically improved oxygen permeability compared to conventional HEMA lenses, significantly reducing hypoxia-related complications. However, due to the stiffness of the material, SEALs may occur, and incompatibility with certain care solutions has been reported to cause donut-shaped superficial punctate keratopathy. Proper care and regular check-ups are important for any CL.
CLs limit the supply of atmospheric oxygen to the cornea. Lenses with low oxygen permeability (Dk/t) increase anaerobic metabolism in the corneal epithelium, leading to epithelial edema from osmotic pressure elevation due to lactate accumulation. In the era of PMMA lenses, epithelial edema localized to the central cornea, known as central circular clouding, was commonly observed.
Conventional HEMA-based SCLs, which were mainstream until around 1990, frequently caused acute epithelial edema due to oxygen deficiency. However, high-Dk silicone hydrogel lenses are now mainstream, and hypoxic complications have decreased.
Chronic hypoxia induces corneal neovascularization. Neovascularization in long-term wearers may reflect potential limbal stem cell deficiency.
Friction between the contact lens and the ocular surface during blinking causes epithelial damage. With HCL, the lens moves approximately 2 mm vertically with each blink, drawing tear fluid from the 3 o’clock and 9 o’clock directions. This depletes tears in those areas, leading to superficial punctate keratopathy. When mechanical stimulation from the lens edge is added, it can progress to corneal erosion and corneal infiltration.
With SCL, friction between the upper eyelid and the CL surface can cause lid-wiper epitheliopathy (LWE) and SEALs. SEALs occur at the site where the upper eyelid presses against the CL and are particularly likely when the corneal side surface of the lens is irregular.
Chronic mechanical stimulation and bacterial endotoxins from CL wear trigger an immune response, leading to sterile infiltrates. This is often caused by inadequately disinfected SCLs or biofilms inside the lens case.
Giant papillary conjunctivitis involves a type I allergic reaction to proteins deposited on the CL surface. Constant contact and stimulation of the upper tarsal conjunctiva by the lens leads to inflammation and formation of giant papillae.
Biofilm formation inside the lens case is an important risk factor for infectious keratitis. Bacteria within biofilms have high resistance to disinfectants, making regular replacement of the lens case essential for prevention.
