Introduction
Contact lens (CL) use has increased tremendously owing to different indications and varied benefits.[1] The common indications for contact lenses are cosmetic use, therapeutic use, treatment of refractive errors, and correction and control of myopia. There are approximately 140 million contact lens users globally, a number that is increasing.[2] Many different types of contact lenses are available in the market to give every patient a spectacle-free life.[3]
Contact lenses act as foreign bodies on the ocular surface and, despite their numerous benefits, are known to cause numerous complications.[4] With improvements in contact lens technology and continued research, the contact lens market has multiplied manifold. Healthcare workers prescribing contact lenses must keep themselves up to date on the benefits and complications associated with contact lenses. The complications can be broadly classified as infective and non-infective, and conjunctival and corneal complications.[5]
The various corneal complications are epithelial edema, microcysts, abrasions, superficial punctate keratitis, contact lens-related peripheral ulceration, peripheral corneal staining, sterile corneal infiltrates, corneal neovascularization, microbial keratitis, bacterial keratitis, fungal keratitis, acanthamoeba keratitis, warpage, and endothelial changes.[6]
The conjunctival complications include allergic conjunctivitis, giant papillary conjunctivitis, and superior limbic keratoconjunctivitis. The other listed complications can be physical damage to the lens and discoloration. CL-related complications have decreased with advances in CL materials, manufacturing techniques, and ocular hygiene. This activity focuses on various problems and complications associated with contact lenses, as well as the necessary interventions to safeguard the patient from irreversible changes.[7]
Function
Tear and Contact Lens Interaction
The corneal tear film plays a vital role in maintaining the functional integrity of the cornea. It acts as a barrier, nourishes, and lubricates the corneal surface. The cornea is the primary refractive surface and comprises numerous refractive elements.[8]
It is vital to maintain the transparency and integrity of the cornea. The contact lens acts as a barrier between the tear film and the cornea, disrupting the harmonious relationship between them. This interaction reduces the health, function, efficiency, efficacy, and acceptability of contact lenses.[9]
Lens Position and Tear Film Interaction
The lens can't be clamped or stuck to the cornea. The properties of the tear film, such as surface tension and viscosity, act as glue to hold the contact lens over the cornea surface.[10] Once the lens is inserted into the eye, the conjunctival mucus rubs against the lens surface during several blinks, and tear fluid helps wet the lens. The tear fluid spreads across the lens surface, including the periphery, and helps adhere the lens to the surface.[11]
The pre-lens tear film acts as a plastic sheet that holds and tacks the lens due to the firm, cohesive forces between water molecules, and also serves as an adhesive between water and the lens material. Approximately 11 grams of force is needed to displace the lens, according to experimental studies. When the tear film covering the lens breaks, the method of internal adhesion plays a key role. Negative pressure builds up between the lens, the corneal surface, and the tear film. It acts as a collar between the edge of the lens and the cornea, and this tear film acts as a container for the lens. When measured, this negative pressure is approximately 29 dynes/ cm.[12]
Optical Properties
The tear lens, or the post-lens tear-film interface, plays an essential role in improving contact lens function.[13] The irregularities on the corneal surface are filled by the tear lens film, thereby forming a uniform optical surface, and the front surface of the tear lens is shaped by the rear surface of the contact lens.[12]
The refractive index of the cornea is 1.376, and that of tears is 1.337. If the indices were equal, all degrees of the irregularities of the corneal surface, as well as astigmatism, would be perfectly corrected with the CL. With high degrees of astigmatism, residual astigmatism will be proportionately higher.[14]
Impact on Corneal Nourishment
Contact lenses impact the cornea in numerous ways.
Retard tear evaporation and reduce tear hypertonicity.
Acts as a barrier to the delivery of oxygen
Traps the water and reduces waste disposal
Injure or traumatize the dead epithelial cells.
[15]
The hard CL covers approximately 50-80% of the corneal surface, and 70-85% of this area is permanently protected by normal lens mobility. The covered area depends on the nutrition of the tear film beneath the contact lens. The post-lens tear interface needs constant renewal to meet the corneal oxygen demands.[16]
It has been observed that under static conditions, the oxygen in the post-lens tear interface is exhausted within 90 seconds with hard or soft CL with 40% hydration. Further, the non-oxygen-dependent pathway is significantly less efficient (approximately 1/18) than the oxygen-dependent pathway. There is an accumulation of lactic acid, which compromises corneal nutrition, resulting in corneal edema and haziness.[13]
The blinking mechanism creates a pumping mechanism at the cornea-contact lens interface, and the pressure on the lid presses the contact lens, expelling the post-lens tear interface, which then forms again. The pump efficacy depends upon
The soft contact lens has a large diameter and comprehensively covers the lens surface. An aqualung effect is observed due to the lens's hydrophilic nature. When blinking is absent, the corneal surface lacks oxygen, and the pump effect is missing. The oxygen delivery in soft lenses is only 10% of that in hard CL. But the lens flexibility helps create a capillary layer of fluid under the lens surface. The corneal deturgescence is reduced due to hypotonicity of the tear film resulting from excessive secretion of tears, change in blink rate, and impairment of evaporation.[17]
Lens Edge Effect
The contact lens is covered by the patient's tear film, resulting in a prism-shaped meniscus at the lens edge. If the edge of the lens enters the pupillary area, it may result in a second focal point of the image on the retina. This is common with both low-riding and high-riding lenses. This is called the ghost image effect or the edge flare effect.[18]
Lens Damage
The lens spoilage can result from irregular contact lens interactions with the tear film. Multiple deposits on the contact lens surface can affect the lens's optical properties. The deposits can damage the contact lens and reduce its working efficiency within six months. The lens deposits can be due to
Lens surface irregularities due to manufacturing defects
Tear film inadequacy
The porosity of the lens
Blink irregularity and deficiency
Immediate tear film break-up time
Altered tear film composition
Reduced tear film volume
Altered pH of the tear film
[19]
Issues of Concern
Corneal Complications
Epithelial Complications
Epithelial Edema
Epithelial edema occurs secondary to hypoxia and is usually reversible. It is one of the commonest and earliest corneal complications.[15]
Microcysts
It occurs due to a long-term decrease in corneal metabolism. They are most commonly seen with soft CL or extended-wear contact lenses. These appear as small dots over the cornea, with varying densities, and may mimic Cogan's microcystic dystrophy. These dots clear once the lens is removed. It is advised that these patients switch from extended wear to daily wear, or from daily wear to gas-permeable lenses.[20]
Abrasions
These are caused by trauma or mechanical injury to the lens or during the insertion or removal of the lens. A foreign body embedded in the lens can also induce corneal abrasions.[21] The patients usually present with pain, redness, and watering, and the abrasions can be delineated on staining. The best treatment is contact lens removal and a course of topical antibiotics. Patching should be avoided in these cases for fear of the eye becoming infected. Once the infection resolves, contact lens wear can be initiated slowly.[22]
Superficial Punctate Keratitis
Superficial Punctate Keratitis (SPKs) occurs due to mechanical injury from the lens or during lens application.[23] Contact lens-induced chemical toxicity also results in SPK. This occurs secondary to preservatives present in the saline, inability to clean the lens properly after using surfactant or enzyme cleansers, or failure to clean or neutralize hydrogen peroxide disinfectants.[24]
The associated ocular pathologies, like dry eyes and blepharitis, can also cause SPKs. Patients with SPK have to stop the lenses until the lesions resolve. The topical antibiotics, lubricating eye drops, and ointments also promote healing. The patient should be reassessed before deciding whether to resume CL wear.[25]
Staining at 3 and 9 o'clock
This occurs due to corneal desiccation because of interruption of the tear film or reduction of the tear film at the nasal and temporal limbus. The main risk factors are poor lens edge tilt, limited lens movement, low-riding lens, poor blink rate, presence of pinguecula, and adherence to the lens surface. It occurs most commonly in RGP lenses.[26]
Sterile Infiltrates
These are due to an inflammatory response to a particular antigen with associated corneal leucocyte infiltration from the adjacent limbal vessels.[27] The preservatives present in the contact lens cleaning solution are implicated as the major source of antigens. These appear as small opacities, which can be epithelial, subepithelial, or anterior stroma.[24] These infiltrates do not cause any symptoms and are detected on a routine examination. In some cases, a corneal infiltrate is an early indicator of microbial keratitis. The infiltrate disappears once the contact lens is discontinued. Once the infiltrate resolves, the patient can start wearing the CL with a preservative-free saline solution.[28]
Peripheral Corneal Ulceration
These ulcers are characterized by epithelial infiltration with an intact Bowman layer. The clinical presentation is different from that of microbial keratitis.[29] The peripheral corneal ulcers involve the paralimbal area, are white, crescentic-to-oval, excavated ulcers, and may be associated with thinning. There is mild congestion and focal infiltrates in contrast to microbial keratitis, which usually affects the visual axis and is characterized by epithelial defect and stromal melt. Peripheral corneal ulceration is also called marginal keratitis, and the primary causative agent is staphylococcal toxins.[30]
Corneal Neovascularization
This results from excessive hypoxia caused by prolonged lens wear or by a tight or thicker lens. Neovascularization can be superficial, deep, sectoral, or involve 360 degrees of the cornea.[4] In extended-wear contact or therapeutic CL, a small amount of peripheral superficial vascularization is common (1-2 mm). A growth having a progression of more than 2 mm or involving a middle or deeper stroma is not common. Careful fitting of CL, regular patient follow-up, and use of high-oxygen-transmission lenses, with discontinuation of older ones, are treatments for neovascularization.[31]
Microbial (Infective) Keratitis
This is also known as contact lens-induced keratitis (CLIK). It is one of the serious complications of contact lens wear, but not a very common one. It may occur with any type of contact lens wear, but is more common with soft CL and more common with extended-wear CL.[4]
It starts with an epithelial defect secondary to trauma or hypoxia associated with microbial contamination. The significant risk factors are poor personal hygiene, inadequate lens cleaning, contamination of the lens cover or lens cleaning solution, and dry eyes and blepharitis. The common organisms involved are Pseudomonas aeruginosa and Acanthamoeba. Other microorganisms, such as Gram-negative and Gram-positive bacteria, can also cause CL-induced keratitis.[4]
Acanthamoeba Castellani Infection
This condition is more common in patients who use homemade saline for lenses, swim in a pool with CL, swim in contaminated water, or are exposed to tap or tub water. The most common clinical features are pain out of proportion to clinical findings, irregularity of epithelium, and patchy stromal infiltrate.[32]
The late clinical features include stromal infiltrate, radial keratoneuritis, and elevated linear epithelial lines. Precautions must be taken to prevent this problem in patients. Prolonged lens wear, primarily sleeping with CL on, is a significant risk factor for Acanthamoeba keratitis. Good ocular hygiene with regular cleaning and disinfection is the critical factor in preventing corneal ulcers in these patients. The patient should be informed in detail about the risk factors and warning signs of corneal infection to avoid this ocular catastrophe. Once a corneal ulcer has developed, it should be addressed promptly and meticulously.[33]
Pseudomonas Aeruginosa Keratitis
Pseudomonas is the most common cause of microbial keratitis in patients using CL. The patient usually presents with pain, redness, and discharge out of proportion to and larger than the infiltrate. The clinical findings include corneal infiltrates, ring infiltrates, and hypopyon in advanced cases.[34]
Fungal Keratitis
Another sight-threatening complication associated with CL is fungal keratitis, characterized by dense gray-white stromal infiltrate, feathery margins, satellite lesions, endothelial exudate, and hypopyon. The diagnosis is made by the corneal scraping of the infiltrate, and smearing and culture will pinpoint the microorganism.[35] The incidence of fungal keratitis secondary to CL wear varies from 10 to 21%. The most common causative agents are Aspergillus, Fusarium, and Candida. CL wear is the major cause of yeast-like fungal keratitis.[36]
Extended-wear lenses are associated with an increased risk of CL keratitis, followed by hydrogel and rigid gas-permeable contact lenses. Trauma with vegetative matter is the major cause, and topical antifungals are the mainstay of treatment. The commonly used antifungals are 5% Natamycin, 0.3% Amphotericin B, 1% Voriconazole, and 1% Itraconazole. Non-resolving cases will require therapeutic keratoplasty.[4]
Warpage
Prolonged contact lens wear can induce severe, permanent astigmatism in response to chronic hypoxia. The corneal shape changes temporarily due to prolonged use of impermeable hard CL. The warpage is usually detected on corneal topography and reverses with the discontinuation of CL. It can also cause a temporary reduction in visual acuity.[37]
Other complications with contact lenses include foreign body tract formation, corneal Dellen, vacuoles, mucin ball formation, and dimple veiling.
Corneal Endothelial Changes
Contact lens wearers can have both short-term and long-term endothelial changes. The endothelial changes are thought to occur secondary to hypoxia, which causes lactic acid accumulation in the cornea, elevated carbon dioxide levels, and reduced pH.[38]
Two types of changes are seen clinically
Endothelial bleb response
This is thought to occur minutes after using a thick, soft, or rigid contact lens. This is a transient effect and doesn't produce other side effects. The bleb changes usually resolve after 30 minutes of lens application or rapidly after lens discontinuation.[13]
Endothelial Polymegathism and Pleomorphism
These changes are noticed after prolonged contact lens wear. These changes are associated with corneal decompensation following intraocular surgery. These changes can be reduced by promoting the use of daily-wear CL over extended-wear lenses and RGP lenses over rigid PMMA lenses.[39]
Contact Lens-Related Discomfort
Per the Tear Film and Ocular Surface Society, discomfort associated with CL is characterized by occasional or regular adverse eye sensations with lens application, which may or may not be accompanied by visual discomfort, secondary to reduced harmony between the CL and the surrounding ocular surface environment.[40]
This results in reduced usage or discontinuation of CL. The CL factors associated with discomfort are lens material, design, wearing time, hygiene, and fit to the ocular surface. The environmental factors are ocular surface changes, occupation, external temperature, humidity, associated medication use, and compliance. The goal of management is to reduce patient discomfort and modify associated factors to enable comfortable daily wear time.[4]
Conjunctival Complications
Allergic Conjunctivitis
This common complication has been reported with thiomersal-containing solutions. The patient presents with pain, redness, itching, and burning sensations. The reaction usually develops after days to months following exposure to thiomersal.[23] The examination reveals conjunctival hyperemia and the papillary response of the conjunctiva. Avoidance of thiomersal is the best treatment, and steroid eye drops should be used in tapering doses to prevent this reaction.[41]
Giant Papillary Conjunctivitis
This is an immunological complication in which the contact lens deposits and proteins act as an allergic stimulus.[23] The main risk factors for GPC include patient susceptibility, contact lens wear schedule, contact lens care regimen, lens material, and design. GPC is more commonly observed after soft CL. Patients with asthma, hay fever, and animal allergy are more susceptible.[4]
The most common symptoms are itching, redness, increased mucus production, photophobia, irritation, and reduction in lens tolerance. The upper palpebral conjunctiva shows giant cobblestone papillae.[42] The GPC can be reduced by avoiding contact lens use, using an enzyme cleanser regularly, changing lenses, avoiding heat disinfectants, and avoiding the use of CL with CL on. The lens should be avoided for at least 1 to 2 months, and the patients should be treated with sodium cromoglycate and steroid eye drops. Once the condition subsides, newer lenses may be fitted to avoid the recurrence.[43]
Superior Limbic Keratoconjunctivitis
Superior limbic keratoconjunctivitis is a hypersensitivity reaction to thiomersal or preservatives in contact lens solution. SLK is usually bilateral and asymmetric.[44]
The patients typically present with pain, redness, foreign body sensation, and contact lens intolerance. The anterior segment findings usually reveal inflammation and hypertrophy of the superior bulbar conjunctiva that stain with Rose Bengal stain, punctate epithelial erosions, microfolds of the superior cornea, and papillary hypertrophy of the superior tarsal conjunctiva. The CL should be discontinued, and lubricating eyedrops should be used frequently. When the pathology resolves, the patient should be given a new pair of contact lenses and must be advised to use non-preserved saline and perform frequent lens cleaning.[44]
Other Issues
Complications Associated With Contact Lenses
Contact lenses can be damaged or spoiled by prolonged use and may cause various problems. There can be physical damage to the lens, a change in lens color, loss of lens, and deposits over the lens.[45]
Physical Damage to the Lens
Damage to the lens can occur as breakage, chipping, or cracking during insertion or removal. The biochemical degradation of the lens also causes physical damage.[4]
Lens Discoloration
This can occur due to systemic use of drugs such as rifampicin, fluorescein, and phenylephrine.[46]
Loss of Lens
This occurs more commonly in the pediatric age group than in adults. Most widely reported with rigid lenses than soft lenses, and more familiar with extended wear lenses than daily wear.[47]
Deposits over Lens
This is another common problem with CL. This is more commonly reported with extended wear, daily-wear soft, RGP, and hard lenses. Deposits can come from the tear film, lens handling, cosmetics, topical drugs, and pollutants such as dust and fumes.[20] The lens deposits occur secondary to poor personal hygiene, lens surface defects, age-related changes, material degradation, and local ocular pathologies such as blepharitis, meibomitis, lagophthalmos, and dry eyes.[25]
The lens deposits can be proteinaceous or lipid-laden. These can cause physical damage to the lens, physiological impairment of gas diffusion, blurred or hazy vision, halos, distortion, polyopia, photophobia, aberrations, and astigmatism. The treatment is to replace lenses when the deposits are clinically significant. The daily-wear lenses should be replaced every 6 months.[48]
