Contact lens complications
There are many complications that the contact lens wearer may experience, either directly induced or ones that represent existing problems aggravated by the contact lens wear. The mechanisms by which the contact lenses induce alterations are: trauma, decreased corneal oxygenation, reduced corneal and conjunctival wetting, stimulation of allergic and inflammatory responses, and infection.
- Pain: all chronic patients using contact lenses may have hypoesthesia.
- Decreased visual acuity: irregularity of the anterior surface of the cornea.
- Conjunctival hyperemia
- Contact lens intolerance
Contact lenses alter the physiology and morphology of the epithelium and can influence corneal integrity. Signs include the following: punctuate epithelial keratopathy, epithelial abrasions, foreign body tracks, dellen, microcysts, vacuoles, mucin balls, dimple veiling. The presence of epithelial defects should be monitored closely, and they may require both temporary cessation of contact lens wear as well as possible prophylactic antibiotic therapy, refitting of contact lenses, and patient education.
This may result from either acute or chronic hypoxic corneal conditions, contact lens materials, and contact lenses that are inadequately fitted. To treat this condition one should select a lens material with higher oxygen permeability, decrease contact lens wearing time, and ensure an optimal contact lens fits.
Alteration of the corneal curvature that results from a molding effect produced by contact lens wear. Treatment consists in making sure there is no irregular astigmatism, contact lens refitting, and change in the material of lens.
All contact lenses reduce corneal sensitivity. Although the exact mechanism for corneal hypoesthesia remains elusive, possible mechanism include:
- Sensitization to the mechanical trauma produced by contact lenses
- Corneal metabolic changes that affect corneal nerves.
Sterile infiltrates represent an immunologic reaction and are a diagnostic dilemma in early keratitis. They may result from contact lens wear itself, from endotoxins created by bacteria or from a combination of the two. Treatment usually consists of prophylactic antibiotic coverage followed by use of topical steroid drops. The infiltrates are usually peripheral and often do not contain an overlying epithelial defect. Close follow-up care, especially early in treatment, should be provided to ensure accurate and early diagnosis of microbial keratitis and to monitor for improvement.
Develops in response to the same inciting factors that causes neovascularization in non-contact lens wearers, including corneal hypoxia and inflammation. For patients with chronic use, neovascularization may represent underlying limbal stem cell deficiency as well. Treatment involves removing the inciting stimuli, and depending on the severity, a pulse of topical corticosteroids to aid in vessel regression.
This is one of the most serious potential complications from contact lens wearing. The incidence is low but contact lens wear is a primary risk factor for developing microbial keratitis. Risk varies based on the type of lens and the wearing schedule.
Overnight use is a leading risk factor, as is extended-wear poor hygiene, and not using appropriate cleaning solutions.   As far as organisms responsible, Pseudomonas Aeruginosa is a common pathogen. Other organisms responsible include Staphylococcus, Streptococcus and Serratia. Another pathogen that is closely related to the use of contact lenses is Acanthamoeba. 88% of patients with Acanthamoeba keratitis (AK) wore contact lenses. AK may be diagnosed through cultures, smears, biopsy or confocal microscopy.
Treatment of microbial keratitis requires immediate and frequent antibiotic coverage with agents susceptible to the offending microorganism. Contact lens use should be immediately stopped. Treatment is based on the severity of the corneal ulcer and whether it appears to be sight threatening or not. Sight threatening ulcers usually include the presence of any of the following characteristics:
- Corneal infiltrate of > 2 mm in size.
- Corneal infiltrate < 3 mm from the visual axis.
- Worsening of clinical course following 48 hours of treatment.
Corneal ulcers that are not sight threatening are empirically treated with fluoroquinolones agents. Vision-threatening corneal cultures and Gram stain should be performed, and broad spectrum antibiotics and cyclopegics should be initiated while culture and sensitivity results are pending. Treatment should be modified as appropriate based on laboratory results and response to initial therapy. Traditionally, Vancomycin and a fortified aminoglycosides (usually Tobramycin) are prescribed hourly. The antimicrobial agents are tapered as wound healing improves, the infiltrate decreases in size, and the inflammatory response improves. Steroid drops may be considered in cases where the culture reveals bacteria (Nocardia, Fungus and Acanthameoba are not amenable to steroids) and there is improvement in infiltrate size and epithelialization after 48 hours of aggressive anti-bacterial therapy. The SCUT trial demonstrated an improvement in visual acuity in patients with non-Nocardia ulcers. 
Treatment of Acanthamoeba keratitis involves a multidrug regimen of anti-amebic drugs, which include polyhexamethylene biguanide, propamidine isethionate and neomycin.
- Boyd K, Pagan-Duran B. Contact Lens-Related Eye Infections. American Academy of Ophthalmology. EyeSmart® Eye health. https://www.aao.org/eye-health/diseases/contact-lens-related-eye-infections-2. Accessed March 07, 2019.
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