Ординатура / Офтальмология / Английские материалы / Contact Lenses in Ophthalmic Practice_Mannis, Zadnik. Coral-Ghanem, Kara-Jose_2003
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edema, decrease in mitosis, delay in epithelial cell turnover, epithelial thinning, and compromised junctional integrity.1–6 By altering the epithelium, contact lenses can challenge corneal health and increase the likelihood for infection, as is demonstrated by the increased incidence of Pseudomonas aeruginosa infections in contact lens wearers compared to non–contact lens wearers.23–25 While most of these changes are subclinical occurrences that occur in normal lens wear, it is critical to monitor for more pronounced changes that further endanger the epithelial integrity.
Conditions of contact lens wear that can further endanger the epithelial integrity include:
1.Inadequate lens oxygen transmissibility
2.Inappropriately fitted contact lens
●Rigid lenses
Excessively flat base curve
Inadequate peripheral edge clearance
Inferiorly decentered
Poorly polished lens or lens edge
●Soft lenses
Tight lens
3.Mechanical trauma secondary to lens insertion or removal
4.Damaged contact lenses
●Deposits on anterior and posterior lens surfaces
●Torn or cracked lenses
5.Debris between lens and cornea
6.Tear film instability
Symptoms and Signs of Epithelial Disruption
Signs include the following:
●Punctate epithelial keratopathy (Color Plate 22)
●Superficial epithelial arcuate line (Color Plate 23)
●Epithelial abrasions
●Foreign body track
●3 and 9 o’clock position desiccation staining
●Dellen (Color Plate 24)
●Microcysts
●Vacuoles
●Mucin balls
●Dimple veiling
Symptoms that may vary based on severity:
●Foreign body sensation
●Photophobia
Treatment of Epithelial Defects
The presence of epithelial defects resulting from contact lens wear must be monitored closely, and treatment may be warranted, depending on
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the severity of the epithelial defect, to prevent against infection. The presence of other clinical signs of epithelial disruption should be followed and modifications to contact lenses should be made to provide the ideal lens fitting relationships. Mucin balls likely are not detrimental to contact lens wear.26 If recurrent epithelial keratopathy persists, subepithelial corneal opacities and scarring may develop in the area of epitheliopathy.
Considerations should include:
●Temporary cessation of contact lens wear
●Prophylactic antibiotic therapy in the presence of epithelial defects
●Refitting of contact lenses
●Patient education
8.What are the causes of corneal hypoesthesia in contact lens wearers?
All contact lens use reduces corneal sensitivity. Some types of lenses are more likely to cause corneal hypesthesia, and historically PMMA lenses are the greatest culprits. Alterations in corneal sensitivity may be acute or chronic and may develop following both short-term and long-term contact lens wear. The consequences of corneal hypesthesia may include an inability to detect painful ocular conditions that signify a potentially threatening situation.
Acute Hypesthesia
●In adapted PMMA lens wearers, corneal sensitivity decreases on average 110% over a 12-hour period following lens insertion.27
●In adapted soft contact lens wearers, placement of a soft lens with a water content of 38% reduces sensitivity approximately half as much as a PMMA lens does.
●The majority of corneal sensation recovery occurs within the first hour for both PMMA and soft lens wearers, but complete recovery in PMMA lens wearers takes longer and is dependent on the cumulative years of lens wear.28–30
Chronic Hypesthesia
Long-term wearers of both soft and RGP contact lenses demonstrate a similar loss of corneal sensitivity.
●The amount of hypesthesia produced in both types of lens wear appears to stabilize after a few months of lens use.31
●Corneal hypesthesia in daily lens wearers does not appear to be dependent on the cumulative years of lens use.31
●In contrast, for PMMA wearers, the duration of lens wear is significantly related to loss of corneal sensitivity.32
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Mechanism of Action
Although the exact mechanisms for corneal hypesthesia remain elusive, possible mechanisms include:
●Sensitization to the mechanical trauma produced by contact lenses. This is most likely the cause of hypesthesia in RGP lens wearers.31
●Corneal metabolic changes that affect corneal nerves. Soft contact lenses most likely produce hypesthesia through this mechanism.31
●Acidosis of the cornea, reducing corneal sensitivity.
Signs and Symptoms of Hypesthesia
●Most patients remain asymptomatic of the hypesthesia. Paradoxically, it may be corneal hypesthesia that allows contact lens wear to be comfortable:
●Lack of pain in contact lens wearers should not be used as a diagnostic factor to rule out complicating conditions when a patient should exhibit pain.
Treatment for Hypesthesia
Utilize high oxygen permeable lens materials when fitting contact lenses.
9.How does contact lens wear alter the endothelium?
Acute Changes: Endothelial Blebs
Edematous endothelial cells can be observed through confocal microscopy and specular reflection following acute hypoxia caused by contact lens use.18
Chronic Changes: Endothelial Polymegethism
Chronic use of contact lenses with low oxygen permeability reduces the uniformity of the endothelial cell size and shape and decreases the total number of endothelial cells.33 While this is generally not visible at the slit lamp, significant changes to the endothelium can reduce the functioning of the endothelial pump and alter corneal hydration.
10.How should contact lens–induced corneal distortion be managed?
Mechanisms of Action
Corneal warpage is an alteration of the corneal curvature that results from a molding effect produced by contact lens wear. It can change the
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refractive error by altering the myopia (or hyperopia), by changing the magnitude or axis of the regular astigmatism, or by inducing irregular astigmatism. It is diagnosed by using corneal topography or keratometry, in which serial curvature changes or topographic (or keratometric mire) irregularity are present. Irregular astigmatism usually causes a decrease in best-corrected spectacle visual acuity that improves with an RGP overrefraction. Irregular astigmatism resulting from corneal disease, such as keratoconus, must be differentiated.
Corneal warpage can result from the wear of any contact lens, but it is more common in certain lens designs:
●Historically, wearers of PMMA lenses were most susceptible to corneal warpage, particularly if they were long-term PMMA wearers. Corneal warpage likely resulted from both a mechanical shape change due to ill-fitting lenses and from focal edematous changes resulting from inadequate corneal oxygenation. Fortunately, few patients still wear PMMA lenses.
●Most patients with normal corneas who wear well-fitted soft and RGP contact lenses do not exhibit corneal warpage, although there are a few exceptions.
●Types of contact lenses that are most likely to cause corneal molding inadvertently include posterior aspheric multifocal RGP lenses and thick, low-water-content soft contact lenses. Both lens types induce warpage due to their fitting characteristics. Posterior surface, aspheric multifocal lenses are traditionally fitted several diopters steep, while thick, low-water-content soft contact lenses frequently exhibit minimal lens movement.
●All types of ill-fitting contact lenses can easily induce corneal warpage.
Treatment of Corneal Distortion
1.In contact lens patients with corneal warpage, it is important to distinguish between the absence and presence of irregular astigmatism and a subsequent decrease in the best-corrected visual acuity.
2.Contact lens refitting should be considered in all patients with a decrease in best-corrected spectacle visual acuity resulting from corneal warpage with irregular astigmatism.
3.For contact lens patients who have corneal molding but do not have irregular astigmatism or a subsequent decrease in spectacle visual acuity, it may not be necessary to refit the contact lens. For example, a presbyopic patient may have superior distance, intermediate, and near contact lens visual acuity using a posterior surface, aspheric RGP design and would be dissatisfied if refitted into a design less likely to induce corneal molding.
Other Types of Corneal Distortion
Other types of corneal distortion that may result from contact lens wear include a corneal impression ring, bulbar conjunctival imprint, and myopia reduction.
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Corneal Impression Ring
An RGP contact lens with an inappropriate peripheral edge lift can cause localized corneal distortion as evident by the presence of an impression ring, or edge imprint. Epithelial compromise may be present as indicated by sodium fluorescein staining. The presence of an impression sign indicates the need to alter the contact lens edge lift or refit the lens entirely. If the remainder of the lens fit is appropriate, the peripheral curvature can be flattened to modify the edge profile and prevent an impression ring.
Bulbar Conjunctival Imprint
Soft contact lenses and large-diameter RGP lenses may produce a conjunctival imprint. The presence of a conjunctival imprint suggests a lens that is excessively tight. If the lens is a soft lens, consider flattening the base curve. In large-diameter RGP lenses producing imprints, the peripheral curves must be flattened.
Myopia Reduction
The ease with which corneal warpage can be induced has led to further development of lens designs to change the shape of the cornea intentionally for temporary myopia reduction. In June 2002, the FDA approved the first (rigid) contact lens for overnight wear in for myopia reduction. The Corneal Refractive Therapy (CRT) Lens, by Paragon Vision Sciences, was approved for all ages for the correction of up to6.00 D of myopia with up to 1.75 D of refractive astigmatism.
11.What are the best methods to prescribe spectacles for contact lens wearers?
Prescribing spectacles in contact lens wearers can be complicated if contact lens–induced corneal warpage is present. Corneal warpage is an alteration of the corneal curvature that results from a molding effect produced by contact lens wear. It can change the refractive error by altering the myopia (or hyperopia), by changing the magnitude or axis of the regular astigmatism, or by inducing irregular astigmatism.
1.If a contact lens wearer desires spectacles for supplemental use and there is neither a decrease in best-corrected spectacle acuity nor complaints of spectacle blur post–lens removal, then glasses should be prescribed based on habitual conditions. There is no reason to delay the manifest refraction after contact lens removal during the examination.
2.In cases where contact lens fitting may induce corneal warpage, such as when using a lens design known to induce corneal warpage or in keratoconus patients, it is advisable to delay writing a spectacle prescription for supplemental use until a few weeks after the contact lens fit has been stabilized.
3.If there is a decrease in best-corrected spectacle visual acuity asso-
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ciated with contact lens–induced corneal warpage, contact lens refitting should be considered. Spectacle prescriptions should ideally be delayed in contact lens refitting until there is a stabilization of the refractive error and a return to the initial best-corrected spectacle visual acuity.
4.In contact lens wearers with stable corneal warpage and no irregular astigmatism or decrease in best-corrected spectacle acuity, it may be appropriate to maintain the same lens design. As discussed earlier, an example may be a presbyopic patient who is satisfied with posterior surface multifocal RGP lenses. Spectacles can be prescribed for supplemental use, and the patient should be informed that cessation of contact lens use may require a change in the spectacle prescription.
12.How and why does corneal vascularization occur, and how should it be managed?
Causes and Mechanism of Action
Corneal neovascularization develops in contact lens wearers in response to the same inciting factors that cause neovascularization in non–contact lens wearers. Some common causes are corneal hypoxia and inflammation. Hypoxia, which can lead to corneal edema, is one of the most common inciting factors in contact lens wearers. Corneal neovascularization most often develops as a result of chronic hypoxia in contact lens wearers (Color Plate 25).
Common Lens Types Associated with Hypoxia
●Tight soft lenses. In patients with borderline dry eyes, a decrease in tear flow can alter the fit of the lens as dehydration occurs. Evaluation of lens fit initially after insertion may demonstrate an appropriate fit, which may become inadequate following several hours of lens wear. Patients are usually symptomatic and describe ocular dryness, an increase in lens awareness, and occasionally a decrease in vision following increased wearing times.
●Thick, low-water content soft lenses.
●PMMA lenses.
●Extended wear of contact lenses that provide insufficient corneal oxygenation in closed-eye conditions.
●Hybrid lenses (hydrogel skirt, rigid center) with low oxygen permeability.
Lens-Related Causes of Inflammation
●Persistent corneal trauma due to an inappropriate lens fit, which can produce corneal changes ranging from mild superficial punctate keratopathy to contact lens–associated acute red eye (CLARE) to cor-
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neal abrasions. Contact lens–induced keratopathies may be severe enough to induce intraocular inflammation, such as iritis.
●Sensitivity reaction to preservatives in lens care products and topical medications.
Symptoms and Signs of Corneal Vascularization
●Clinically, superficial corneal vascularization should be distinguished from deep stromal vascularization, and documentation should include measurement with the slit lamp. Contact lens– associated neovascularization is superficial and extends more than 1 mm beyond the limbus in only 10% of contact lens patients.34 Vascular patterns in which a spike, branch, or sprout is present at the end of the vessel should be closely monitored for progression.35 The formation of neovascularization is a static process consisting of remodeling changes, so recently formed vessels can regress if the inciting factor is removed early enough in the formation of the vessel. Established vessels do not regress, and treatment of the condition results in a patent vasculature without red blood cells. These vessels, called ghost vessels, can rapidly refill with red blood cells in the presence of hypoxic or inflammation stimuli.36
●Associated findings present with corneal neovascularization may include the presence of adjacent ghost vessels, early corneal opacification, corneal exudate, limbal hyperemia, and conjunctival injection.
Treatment of Corneal Vascularization
The goal in the management of corneal neovascularization is for the vessels to empty of red blood cells and become ghost vessels. If treated early enough in the neovascularization process, all clinical signs of vessels in the cornea should resolve.36
Treatment involves removing the inciting stimuli. This may include the following:
1.Change to a more highly oxygen permeable lens material.
2.Reduce contact lens wearing time.
3.Improve the lens-to-cornea fitting relationship to prevent corneal keratopathy.
4.Treat any preexisting conditions that may be adding to the corneal keratopathy, such as blepharitis.
5.Switch lens care products if a toxic reaction resulting from hypersensitivity is suspected.
6.In the presence of moderate-to-severe inflammation, consider a pulse of topical nonsteroidal antiinflammatory drugs (NSAIDs) or corticosteroids to aid in vessel regression.
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13.What is the appearance of toxicity reactions in the cornea?
Causes and Mechanism of Action
Toxicity reactions from contact lens care products and topical ophthalmic medications may result if a hypersensitivity exists to the offending agent. Historically, many contact lens care products contained preservatives that produced toxic reactions. The use of most of these preservatives has been discontinued, and toxicity reactions are not nearly as common today. Thimerosal, a mercury-containing preservative, is regarded as a primary cause of toxic corneal reactions, and is rarely used anymore in ophthalmic products.37 Benzalkonium chloride (BAK) is still used as a preservative in many topical ophthalmic medications and in some lens care products, but it does not cause hypersensitivity reactions as frequently as thimerosal.
Signs and Symptoms of Toxicity Reaction in the Cornea
Thimerosal toxicity reactions may produce a variable clinical picture, which may include:
1.Superificial punctate keratopathy.
2.Pseudodendrites (Color Plate 26): Appearance similar to dendrites produced by herpes simplex keratitis without the terminal bulbs. Lesions stain with sodium fluorescein dye.38
3.Subepithelial corneal opacities39: Similar in appearance to other causes of subepithelial opacities, including viral, bacterial, and chlamydial.
4.Contact lens–associated superior limbic keratoconjunctivitis (Color Plate 27)40: Similar entity to the superior limbic keratoconjunctivitis described by Theodore and Ferry,41 but occurs in younger patients without history of thyroid disorder.
Treatment of Toxicity Reaction in the Cornea
1.Toxicity reactions require a discontinuation of the offending agent.
2.Consider therapeutic agents, such as anti-inflammatory medications, if sufficient inflammation exists, or prophylactic antibiotics, if significant epithelial involvement is present.
14.What types of keratitis can result from contact lens use?
While all types of keratitis can present in contact lens wearers, two main types of ulcerative keratitis are particularly associated with contact lens use. These are microbial keratitis, namely Pseudomonas aeruginosa and Acanthamoeba keratitis. Both can have significant visual morbidity. The
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following section discusses sterile marginal infiltrates, microbial keratitis including that caused by P. aeruginosa (Color Plate 28), and Acanthamoeba keratitis (Color Plate 29). These are the main types of keratitis resulting from contact lenses. Other types of keratitis (i.e., viral, herpetic fungal, parasitic, etc.) are not included in this discussion, as they are less commonly associated with contact lens use, but they should be considered in the list of differentials in any keratitis.
15.How is microbial keratitis differentiated from sterile marginal infiltrates, also known as contact lens peripheral
ulcers (CLPUs)?
One of the most serious potential complications from contact lens wear is microbial keratitis, or a bacterial corneal ulcer. Although the incidence of microbial keratitis is low, contact lens wear is the primary risk factor for developing microbial keratitis, and the risk varies based on the type of lens and the wearing schedule. The estimated annualized incidence of microbial keratitis is 1.1 per 10,000 users of daily wear RGP lenses, 3.5 per 10,000 users of daily wear soft lenses, and 20.0 per 10,000 users of extended wear soft lenses (p .00001 for comparison between all groups).42 In traditional soft hydrogel lens materials, the relative risk for corneal ulcers is 10 to 15 times greater when lenses are worn for extended periods of time as compared to daily wear.43 No studies have reported either the annualized incidence of microbial keratitis with silicone hydrogel ultrahigh Dk lenses or the relative risk for microbial keratitis in extended wear compared to daily wear silicone hydrogels.
While the incidence of microbial keratitis is very low, correctly differentiating microbial keratitis from sterile marginal infiltrates is critical to avoid potentially sight-threatening consequences. Sterile marginal infiltrates represent the greatest diagnostic dilemma to early microbial keratitis, and they are generally considered to be an immunologic response. Sterile marginal infiltrates may result from contact lens wear itself, from endotoxins created by bacteria present in conditions such as Staphylococcus aureus–associated blepharitis, or from a combination of the two.44,45 Because virulent strains of microbial keratitis can perforate a cornea rapidly, accurate diagnosis and immediate management of microbial keratitis is crucial.
Clinical differentiating characteristics are as follows:
Sterile Marginal Infiltrates (Color Plate 30)
Stromal infiltrate characteristics include the following:
●Focal infiltrate, primarily anterior stromal.
●Diameter of infiltrate usually ranges from 0.1 to 1.2 mm.45
●Peripheral or mid-peripheral corneal involvement; infiltrates are
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usually 2.5 mm or less from the limbus and involves a ‘‘clear zone’’ of cornea between the infiltrate and limbus.45
●Absence of overlying epithelial defects except in more severe cases.
●Absence of associated corneal thinning.
●Absence of cell, flare, or other inflammation in the anterior chamber.
●Minimal decrease in visual acuity.
●Minimal subjective pain.
Microbial Keratitis
Stromal infiltrate characteristics include the following:
●Stromal involvement may extend to deep stromal layers, with the exception of early ulcers.
●Presence of an epithelial defect. Although nearly all cases of microbial keratitis have an epithelial defect present, this is not an absolute rule. Culture-positive cases of microbial keratitis without epithelial ulceration have been reported, with the offending microorganisms representing both gram-positive and-negative organisms.46
●Central and paracentral involvement.
●Presence of corneal thinning, edema, necrosis, or neovascularization. Other characteristics include:
●Presence of anterior chamber inflammation, including cell, flare, and hypopyon, which may result in miosis and posterior synechiae. Ability to assess the anterior chamber inflammation may be decreased due to the presence of a dense infiltrate.
●Significant decrease in visual acuity.
●Significant subjective pain.
16.What is the management of sterile infiltrates?
Sterile infiltrates represent an immunologic reaction (Color Plate 30).44 Treatment usually consists of topical steroid drops along with prophylactic antibiotic coverage. For most cases, dosing four times daily is adequate, although dosing with increased frequency may be appropriate if multiple sterile infiltrates are present. Close follow-up care, especially early in treatment, should be provided to prevent inappropriate treatment of an early microbial keratitis and to monitor for improvement. Improvement usually occurs quickly following steroid initiation. While the diagnosis and treatment of the acute condition is of primary concern, it is critical to evaluate and treat thoroughly any chronic ocular surface disease, such as blepharitis or dry eye syndrome, which may increase the likelihood for future recurrence or additional complications.
