Topographic changes in contact lens-induced corneal warpage

Twenty-one eyes of 12 patients with contact lens-induced corneal warpage were followed prospectively using computer-assisted topographic analysis. Sixteen eyes had worn rigid contact lenses (13 eyes, polymethylmethacrylate; three eyes, gas-permeable), and five eyes had worn soft contact lenses. Initial corneal topographic patterns were characterized by the presence of central irregular astigmatism, loss of radial symmetry, and frequent reversal of the normal topographic pattern of progressive flattening of corneal contour from the center to the periphery. A correlation was noted between the initial corneal topography and the resting position of the contact lens on the cornea for nine of the 16 eyes with rigid contact lenses. Initial topography for each of these corneas showed relative flattening of the corneal contour underlying the resting position of a decentered contact lens. Superior-riding lenses produced a topography that simulated early keratoconus. After cessation of contact lens wear, 16 of 21 eyes had a change in corneal shape to a topography that was consistent with a normal pattern. Five corneas stabilized with an abnormal topographic pattern. A much longer time without contact lenses than had been previously reported, up to 5 months, was required for a return of a stable corneal topography in eyes with contact lens-induced corneal warpage caused by rigid lenses.     

Time to resolution of contact lens-induced corneal warpage prior to refractive surgery.

PURPOSE: To evaluate the resolution of contact lens-induced corneal warpage before keratorefractive surgery. METHODS: We prospectively studied the eyes of 165 consecutive contact lens-wearing patients evaluated for keratorefractive surgery. Significant contact lens-induced corneal warpage was detected by comeal topography in 20 eyes of 11 patients. Manifested refraction, keratometry, and cornea topography were subsequently recorded during weekly or biweekly reevaluations and were compared with previous measurements for stability. Effects of age, sex, type, and duration of contact-lens wear and the recovery time period to stabilization were analyzed. RESULTS: Overall, a 12% incidence of significant contact lens-induced corneal warpage was found. In patients demonstrating lens-associated warpage, the mean duration of prior contact lens wear was 21.2 years (range 10 to 30 years); lens use included daily wear soft (n=2), extended-wear soft (n=6), toric (n=4), and rigid gas-permeable contact lenses (n=8). Up to 3.0 diopter (D) refractive and 2.5D keratometric shifts accompanied by significant topography pattern differences were observed. The average recovery time for stabilization of refraction, keratometry (change within +/- 0.5D), and topography pattern was 7.8+/-6.7 weeks (range 1 to 20 weeks). Recovery rates differed between the lens types: soft extended-wear 11.6+/-8.5 weeks, soft toric lens 5.5+/-4.9 weeks, soft daily wear 2.5+/-2.1 weeks, and rigid gas-permeable 8.8+/-6.8 weeks. CONCLUSION: We observed a 12% incidence of significant contact lens-induced corneal warpage in patients undergoing evaluation for keratorefractive surgery. Warpage occurred with all types of contact lens wear but resolved at different rates. To optimize the quality and predictability of keratorefractive procedures, an appropriate waiting period is necessary for contact lens-induced corneal warpage to stabilize. We suggest that resolution of corneal warpage be documented by stable serial manifested refractions, keratometry, and corneal topographic patterns before scheduling patients for keratorefractive surgery.     

Contact lens-induced corneal endothelial polymegathism: functional significance and possible mechanisms

The corneal endothelium is principally responsible for maintenance of corneal deturgescence. Therefore, compromise of corneal endothelial functional integrity can result in corneal swelling and opacification. Contact lenses constitute a potential insult to the cornea because their wear reduces the oxygen available to that tissue. It has been reported that contact lens wear induces transient as well as permanent morphologic changes in the corneal endothelium. One of the permanent changes reported is referred to as polymegathism, which is a variation in cell size within the endothelial monolayer. Several investigators have suggested that polymegathism reflects a compromised endothelial functional status. Mechanisms proposed to explain contact lens-induced polymegathism include lactate accumulation, changes in pH, and elevation in CO2 content. We discuss these possibilities as well as speculate that these polymegathous shape changes may be a result of decreased endothelial ATP (adenosine triphosphate) levels and disturbed calcium homeostasis due to corneal endothelial hypoxia.     

Contact lens-induced corneal swelling and surface changes measured with the Orbscan II corneal topographer.

PURPOSE: The purpose of this study was to measure central and topographical corneal swelling in response to contact lens wear and eye closure, to determine whether the swelling induced by soft and polymethyl methacrylate (PMMA) lenses is different, and to determine whether the anterior and/or posterior corneal shape alters with corneal swelling. METHODS: An Orbscan II corneal topographer was used to measure corneal swelling and the shape of the anterior and posterior corneal surfaces of 16 neophytes before and after wearing soft and PMMA contact lenses with near-zero oxygen transmissibility. The lens-wearing eye was patched for 3 h. RESULTS: The mean 15.1% +/- 3.8% (+/- SD) central corneal swelling with soft lenses was significantly >12.6% +/- 4.1% with PMMA lenses. Topographical corneal swelling was significantly greater with soft vs. PMMA lenses. However, the difference between central and peripheral corneal swelling was much greater with PMMA lenses. With both lenses, the cornea swelled significantly more in the center than the periphery. The anterior best-fit sphere radius remained unchanged in response to soft lenses (0.00 +/- 0.04 mm) and steepened slightly but significantly with PMMA lenses (-0.04 +/- 0.05 mm). The posterior best-fit sphere radius flattened significantly with both lenses (0.12 +/- 0.07 mm with soft and 0.14 +/- 0.08 mm with PMMA lenses). CONCLUSIONS: Corneal swelling (greater centrally than peripherally) flattens the posterior surface of the cornea and is independent of lens type. Although the anterior best-fit sphere radius steepened with PMMA, the magnitude is probably clinically unimportant. Both lens types produced greater central vs. peripheral corneal swelling. However, the soft lens induced significantly greater overall swelling than PMMA. Because their oxygen transmission was the same, these results suggest that there is lateral diffusion of oxygen from the peripheral area of the cornea (that is not covered by the lens) toward the center.     

Present status of contact lens-induced corneal infections

This article addresses the spectrum of corneal infections associated with contact lens wear. The status of bacterial, fungal, and Acanthamoeba keratitis is discussed as well as diagnosis and treatment for these infections.     

Contact lens-induced pseudo-dystrophy of the cornea?

Whitish dots in the stroma of the cornea resembling the cloudy dystrophy were observed in 4 patients wearing HEMA contact lenses; a lattice-like corneal pattern was seen in another patient wearing HEMA contact lenses. There were no complaints. Visual acuity was normal. Corneal sensitivity was normal or reduced. The pseudo-dystrophies vanished after replacement of the HEMA lenses by Boston IV material.     

Hard contact lens-induced corneal neovascularization treated by oxygenation.

A 39-year-old man suffered from corneal neovascularization, through to result from hypoxia caused by improper use of polymethylmethacrylate (PMMA) hard contact lenses. The condition was successfully treated by oxygenation of the corneas under swimming goggles.     

Contact lens-induced edema in vitro--amelioration by lactate dehydrogenase inhibitors

Isolated rabbit corneas bathed in Krebs-bicarbonate Ringer solution were observed for thickness changes after a 90 minute equilibration period. Control corneas swelled an average of 0.5 micron/hr, and placement of a polymethylmechacrylate (PMMA) contact lens on the epithelial surface caused the corneas to swell 24.5 microns/hr, an effect similar to 0.5 mM epithelial cyanide exposure. The pronounced swelling induced by PMMA lens placement was much less however, in the epithelial presence of 3.2 mM sodium oxalate (3.22 microns/hr) or 3.2 mM sodium oxamate (5.38 microns/hr). An equiosmotic excess of 4.8 mM NaCl was least active (15.89 microns/hr). On normal isolated corneas (without contact lenses), the Ringer containing an excess of 4.8 mM NaCl significantly deswelled the corneas (-13.44 microns/hr), which contrasted with oxalate and oxamate containing Ringer solutions (1.17 and 1.33 micron/hr respectively). The present study supports the notion that contact lens-induced edema results from stromal lactate accumulation, and suggests a potential alternative to osmotic therapy for its amelioration. These LDH inhibitors, in the concentrations used, have no acute osmotic or toxic effect on normal corneas in vitro.     

Contact lens-induced edema in vitro. Pharmacology and metabolic considerations

The effects of physiologic and pharmacologic manipulations on contact lens-induced edema were studied. In isolated superfused rabbit corneas bathed in Ringer's solution and covered with large-diameter polymethylmethacrylate (PMMA) lenses, corneal swelling rates of 17-26 microns/hr (versus -5-5 microns/hr in paired controls) were observed. Neither the calcium antagonist diltiazem (10(-4) M), the glucocorticoid dexamethasone (10(-7) M), the glucose substitute fructose (20 mM), nor 0.5 mM adenosine and 0.3 mM reduced glutathione mitigated the edema. Lens-induced edema was 25 microns/hr in corneas bathed at pH 8.2 and decreased to 9 microns/hr at pH 7.0. In corneas without lenses, however, decreasing the pH from 7.4-7.0 caused significant swelling (P less than 0.05). The pyruvate dehydrogenase stimulant sodium dichloroacetate (3.2 mM) on the tears side ameliorated the edema, and its congener, 3.2 mM 2-chloropropionate, was less effective. These latter agents are known to relieve lactic acidosis systemically and had no significant effect on corneas without lenses. In tissues bathed with 20 mM lactate Ringer's, normal thickness was maintained in both control and PMMA-treated corneas throughout the 3-hr period. These findings suggest that the contact lens-induced edema does not involve the acute cytotoxic mechanisms seen in severe tissue ischemia or hypoxia. The edema appears to result in part from acidosis but mainly from stromal lactate accumulation.     

Contact lens-induced infection--a new model of Candida albicans keratitis.

PURPOSE: A model of experimental keratomycosis was established that mimics human disease in which the only fungi present are those that are actively growing within the cornea. METHODS: Dutch-belted rabbits received a subconjunctival injection of triamcinolone acetonide to one eye. One day later the epithelium was removed from the central cornea and a standardized inoculum of Candida albicans blastoconidia was placed on the corneal surface and covered with a contact lens. The lids were closed with a lateral tarsorrhaphy. After 24 hours, the lid sutures and contact lens were removed. Five days later the animals were killed, and their corneas were subjected to separate isolate recovery and histology studies. A group of similarly infected rabbits without corticosteroid injection served as controls. RESULTS: Both groups developed invasive corneal disease. Although isolate recovery was not significantly different from corticosteroid-treated rabbits compared with controls, fungal biomass was increased. Hyphal invasion was limited to the anterior cornea in control eyes, but penetrated deep stroma in most of the corticosteroid-treated rabbits. CONCLUSIONS: Invasive corneal disease can be established with a surface inoculum. Corticosteroid administration increased corneal penetration of hyphae. Quantitative isolate recovery is not a reliable measure of the fungal load within the cornea.     

Corneal thickness indices discriminate between keratoconus and contact lens-induced corneal thinning

PURPOSE: To evaluate two indices generated from measurements obtained from the Orbscan Corneal Topography System (CTS; Orbscan, Inc., Salt Lake City, UT) to distinguish contact lens-induced corneal thinning from keratoconus. The corneal thickness index (CTI) was used to compare central and peripheral corneal thicknesses. The discriminant function 1 (DF1) was used to evaluate corneal thickness and central keratometry measurements. DESIGN: Case-control study. PARTICIPANTS: Fifty-four patients with keratoconus or suspected keratoconus, 75 contact lens wearers, and 67 normal controls. METHODS: In the initial model-building study, the central and peripheral corneal thickness and central keratometry (K) readings were evaluated retrospectively in 1 eye each of 23 patients with clinically defined keratoconus, 31 contact lens wearers, and 43 normal patients with the Orbscan CTS. Two methods (corneal thickness index [CTI] and discriminant function 1 [DF1]) were evaluated for their efficacy in classifying these conditions. The CTI was designed as the ratio between mean peripheral corneal thickness and the central corneal thickness, and the formula for the DF1 was as follows: DF1 = 0.044 x central thickness - 0.030 x nasal thickness + 9.210 x CTI - 0.157 x Max K - 8.9. In the subsequent validation study, the results were verified in a separate group of keratoconus patients (n = 23), keratoconus suspects (n = 8), contact lens wearers (n = 44), and normal patients (n = 24). MAIN OUTCOME MEASURES: Corneal thickness index (CTI) and discriminant function 1 (DF1). RESULTS: The corneal thickness in patients with keratoconus and contact lens wearers was significantly thinner than that of normal eyes in the central and eight peripheral measured sites (P < 0.001). The corneal thickness in contact lens wearers was significantly greater than in keratoconus patients in the inferotemporal (P = 0.013), inferior (P = 0.003), and central (P < 0.001) sites and was borderline different in the superior site (P = 0.07). In the model-building study, the CTI in keratoconus patients (1.28 +/- 0.15) was significantly greater than in contact lens-wearing (1.10 +/- 0.03; P < 0.001) and normal eyes (1.09 +/- 0.04; P < 0.001). The CTI was not significantly different between normal and contact lens-wearing eyes (P = 0.68). A CTI value of 1.16 or more showed a sensitivity of 91% and specificity of 99% in differentiating keratoconus from contact lens-wearing and normal eyes. The DF1 value was significantly lower in keratoconic eyes than in contact lens-wearing and normal eyes. A DF1 value of -0.6 showed a 96% sensitivity and 99% specificity in differentiating keratoconus from contact lens-wearing and normal eyes. Similar results were obtained in the validation study. CONCLUSIONS: Corneal thickness indices generated from the Orbscan CTS appear to be sensitive and specific for diagnosing keratoconus. These indices may prove to be clinically useful parameters for distinguishing keratoconus from contact lens-induced corneal thinning.     

Contact lens-induced edema in vitro. Ion transport and metabolic considerations

The relationship of contact lens-induced edema to epithelial and endothelial function was determined in isolated superfused rabbit corneas. Placement of a polymethyl methacrylate (PMMA) contact lens on the cornea caused swelling rates of 15-28 microns/hr compared to 0-6 microns/hr in paired control corneas. The edema increased with temperature (P less than 0.01). PMMA-induced swelling was significant in: 1) bicarbonate-free Ringer's solution; 2) chloride-free Ringer's; 3) 0.3 mM furosemide-treated corneas; and 4) deepithelialized corneas. The swelling did not occur in corneas with silicone oil replacing the endothelium to block fluid uptake. The effluent aqueous bathing fluid from edematous corneas did not induce edema in normoxic corneas. These studies demonstrate that contact lens-induced edema depends on metabolism, involves a significant stromal contribution, and requires fluid absorption across the endothelial layer, but is not a direct result of epithelial and endothelial ion transport inhibition.     

Inhibition of contact lens-induced corneal neovascularization in radial keratotomized rabbit eyes

Cellulose acetate butyrate contact lenses were fitted for extended wear on 28 rabbits 6 weeks after radial keratotomy. Fourteen rabbits received 0.03% flurbiprofen to one eye and vehicle solution to the contralateral control eye, while the other 14 received 1% prednisolone acetate to one eye and vehicle solution to the contralateral control eye four times each day in a double-blind fashion. The eyes were photographed and graded weekly with a standardized slit-lamp grading method. After 6 weeks, inhibition of corneal neovascularization was found with flurbiprofen (p = 0.001), while there was a trend toward inhibition of corneal neovascularization with prednisolone acetate (p = 0.076). We also found a significant vehicle effect, with hydroxypropyl methylcellulose, the more viscous vehicle, suppressing corneal neovascularization more than polyvinyl alcohol (p = 0.004).     

Contact lens-associated corneal infiltrates

PURPOSE This review article examines recent studies pertaining to contact lens-associated corneal infiltrates (CLACI) that occur in the absence of culture-proven microbial infection. METHODS The literature was reviewed in regard to the clinical appearance, incidence and risk, etiology, pathophysiology, differential diagnosis, and management of CLACI. Recent insights are presented in the context of future directions for prevention of CLACI. RESULTS Contact lens-associated corneal infiltrates may manifest in various forms that require careful observational skills to ensure proper diagnosis. Although the reported incidence of CLACI varies widely, even a low percentage of contact lens wearers would constitute a substantial number of affected individuals. Any one or a combination of multiple mechanical, hypoxic, or toxic stimuli associated with contact lens use can induce proinflammatory responses that lead to infiltration of inflammatory cells into the cornea. A number of candidate cytokines, chemokines, adhesion molecules, and so forth have been identified. In addition to differentiation from microbial keratitis, CLACI also should be differentiated from ocular disorders not associated with contact lenses but involving corneal infiltrates and from contact lens-associated disorders that may resemble infiltrates. Management of CLACI can range from simple monitoring of the patient to the use of pharmacologic intervention. CONCLUSIONS The small percentage of affected lens wearers translates into a notable number of individuals who, although not experiencing a vision-threatening event, are inconvenienced by the development of infiltrates. Design of preventive measures for CLACI should focus on the elimination of various mechanical, hypoxic, and toxic stimuli that can induce infiltrates and on the approaches for molecular intervention of the inflammatory cascade initiated by the stimuli.     

Simultaneous bilensectomy and endothelial keratoplasty for angle-supported phakic intraocular lens-induced corneal decompensation

A 40-year-old lady presented with severe endothelial cell loss in both eyes 14 years after angle-supported phakic intraocular lens (AS PIOL) implantation. The left eye had severe corneal edema with bullous keratopathy. The right eye had markedly reduced endothelial cell count (655 cells/mm 2 ) although the cornea was clear. She underwent simultaneous bilensectomy (AS PIOL explantation and phacoemulsification) and Descemet's stripping and endothelial keratoplasty (DSEK) in the left eye. Explanted AS PIOL was identified as ZSAL-4 (Morcher, Stuttgart, Germany) model. Corneal edema cleared completely in 2 months with a best corrected visual acuity (-2.25 D sph) of 20/60. No intervention was done in the right eye. The present case illustrates that AS PIOL-induced endothelial decompensation can be effectively managed by simultaneous bilensectomy and endothelial keratoplasty.