Search

Purpose: To investigate the effect of various oxygen transmissibilities (Dk/t) of scleral lenses and corneal thickness recovery time from overnight eye closure with patching on corneal edema during 5 h lens wear., Methods: Scleral lenses (hofocon A, 15.6 mm diameter) were worn bilaterally with three different Dks (100, 140, and 160 Barrer). Central and peripheral corneal thickness (CCT and PCT) were measured using optical coherence tomography. Four subjects were randomly selected for one additional visit and asked to patch one eye before night sleeping. The patch was not removed until lens insertion to avoid corneal deswelling. Then CCT of both eyes was measured., Results: Ten neophytes with healthy eyes participated in the study. Mean [95% CI] Dk/t of the study lenses was 32.0 [29.2, 34.7] hBarrer/cm. Mean [95% CI] CCT immediately upon lens insertion and after 5 h of lens wear were 532.4 [520.3, 544.5] μm and 538.7 [526.5, 551.0] μm, respectively. Mean [95% CI] percentage change (%Δ) in CCT was 1.2% [0.9%, 1.5%], 1.2% [0.9%, 1.4%], and 0.8% [0.6%, 1.1%] for CCT, nasal PCT, and temporal PCT, respectively. There was an inverse relationship between temporal Dk/t and %ΔPCT (p < 0.05) while Dk/t was not found significantly associated with either CCT or nasal PCT. The patched eyes maintained a relatively stable CCT and showed progressive deswelling, starting and ending with 2.8% and 0.6%, respectively. In contrast, the unpatched eyes swelled, starting with nearly 0% and ending with 0.7% with a maximum swelling of 1.8%., Conclusion: There was limited amount of corneal edema induced by short-term scleral lens wear with lens Dk/t ranging from 21 to 47 hBarrer/cm and lenses with lower lens Dk/t did not induce significantly higher corneal swelling. Scleral lens insertion soon after overnight eye closure with patching did not introduce additional swelling for young and healthy eyes., (Copyright © 2019 British Contact Lens Association. Published by Elsevier Ltd. All rights reserved.)

Purpose: To evaluate the safety of scleral-lens designs, we model and clinically assess central corneal edema induced by scleral-lens wear for healthy subjects., Materials and Methods: Central corneal swelling during scleral-lens wear is measured using optical coherence tomography (OCT). Transport resistances are modeled for oxygen diffusion through the scleral lens and post-lens tear-film (PoLTF), and into the cornea. Oxygen deficiency in the cornea activates anaerobic metabolic reactions that induce corneal edema. Oxygen permeability, carbon-dioxide permeability, settled-lens PoLTF thickness, and scleral-lens thickness are varied in the calculations to mimic different lens fits., Results: Transport modeling predicts that for open eyes, increasing PoLTF thickness from 50 to 400 µm increases central corneal swelling by approximately 1-1.5% when oxygen transmissibility (Dk/L) is greater than 10 hBarrer/cm (i.e., hectoBarrer/cm). Although swelling is larger for oxygen Dk/L < 10 hBarrer/cm, PoLTF thickness has minimal impact in this range. For open eye, oxygen transmissibility of the lens plays a significant role in corneal edema, but is negligible when oxygen Dk/L is > 40 hBarrer/cm. For closed eye, central corneal swelling is greater than 5% for an oxygen Dk/L range of 0-100 hBarrer/cm with typical lens-fitting parameters. For carbon-dioxide transmissibilities increasing from 50 to 250 hBarrer/cm and with a fixed oxygen Dk/L of 25 hBarrer/cm, calculated swelling diminishes by an additional 0.5%. Comparison of model calculations to clinical-swelling data is within the error range of the clinical measurements., Conclusions: Oxygen/metabolite transport calculations for open-eye scleral-lens wear show that typical PoLTF thicknesses fitted by clinicians (i.e., PoLTF thicknesses < 400 µm) with modern scleral lenses (i.e., oxygen Dk/L > 25 hBarrer/cm) produce corneal swelling of less than 2% in agreement with experiment. Therefore, scleral lenses prescribed today evoke less than physiological hypoxic swelling (i.e., less than 4%) for healthy corneas during open-eye. Closed-eye wear, however, appears clinically unsafe.

Purpose: To determine if the variability in contact lens-induced corneal swelling is associated with variability in corneal oxygen consumption (Q(C)) or corneal endothelial function., Methods: Corneal swelling was induced in 30 non-contact lens wearers by 2 hours of closed-eye contact lens wear, using thick (oxygen transmission [Dk/t] = 4.0 x 10-9) and thin (Dk/t = 12 x 10-9) hydrogel lenses of identical design. Following the induction of swelling, corneal thickness was continually measured by pachymetry until open-eye steady-state (OESS) thickness was achieved. The percentage of recovery per hour was calculated as a measure of endothelial function. Tear oxygen tension (PO(2)) beneath the hydrogels was measured in the open eye and after 5 minutes of eye closure to obtain estimates of Q(C). A change in corneal pH during eye closure while wearing the hydrogels was used as a measure of hypoxic acidosis. Associations between corneal swelling and endothelial cell density or corneal epithelial thickness were also tested., Results: There were modest but significant (P < 0.05) correlations between thick-lens corneal swelling and thick-lens closed-eye PO(2) (r = -0.36); thin lens corneal swelling and thin-lens closed-eye and open-eye PO(2) (r = -0.40 and -0.39, respectively). Corneal swelling also increases with increasing Q(C) (r = + 0.29 to + 0.33). Corneal swelling was associated with the decrease in pH during lens wear (r = + 0.30 and + 0.20 for thick and thin lenses, respectively). Thick- and thin-lens corneal swelling was significantly associated with percentage of recovery per hour (r = -0.40 and -0.34, respectively). Multiple regression analysis of corneal swelling with PO(2) and percentage of recovery per hour suggested an additive effect, however the effects were not significant. There was a modest inverse association between corneal swelling and OESS, however there were no associations between corneal swelling and endothelial cell density or epithelial thickness., Conclusions: The variability in contact lens-induced corneal swelling is associated with both corneal metabolic activity (Q(C) and pH) and endothelial function (percentage of recovery per hour). Our interpretation is that individuals with larger Q(C) produce more lactic acid (i.e., more swelling) whereas stronger endothelial function resists swelling. The modest correlations, however, suggest that other factors also are involved in explaining the phenomenon of corneal swelling.

Contact lens wear can cause a number of physiological changes in the cornea. Two areas of interest in my laboratory have been contact lens effects on the endothelium and, more recently, the role of metabolic activity in predicting corneal swelling. The first part of this review focuses on the function of the corneal endothelium, the nature of its fluid pump, and the effects of contact lens-induced hypoxia and corneal pH changes on corneal endothelial function. In the second part, the etiology of hypoxia-induced corneal swelling is reviewed in relation to new studies on the causes of intersubject corneal swelling variability. The results indicate that corneal swelling is influenced by both corneal metabolic activity and endothelial function.

Purpose: To study the effects of long-term contact lens wear on morphologic and physiologic properties of corneal endothelial cells., Methods: The endothelial permeability to fluorescein and the rate of corneal deswelling from hypoxia-induced edema were measured in 20 long-term (mean, 17+/-9 years; range, 5-33 years) contact lens wearers and 20 age-matched control subjects. From these data, the relative endothelial pump rate in each subject was estimated, based on the pump-leak hypothesis of corneal hydration control. Corneal autofluorescence and the aqueous humor flow rate were determined by fluorescein fluorophotometry. Images of corneal endothelial cells were recorded by using specular microscopy, and morphologic indices (cell density, coefficient of variation of cell area, percentage of hexagonal cells, and skewness) were determined., Results: No statistically significant differences were found between the contact lens and control groups in endothelial permeability, corneal deswelling, relative endothelial pump rate ([mean +/- SD] 1.07+/-0.33 relative pump units versus 1.01+/-0.25 relative pump units; contact lens versus control; P = 0.57), and endothelial cell density. Contact lens wearers had a significantly higher aqueous humor flow rate (3.57+/-1.03 microl/min versus 2.77+/-0.51 microl/min; P = 0.005), coefficient of variation of cell area (0.35+/-0.09 versus 0.28+/-0.04; P = 0.006), and corneal autofluorescence (3.1+/-0.6 ng/ml versus 2.3+/-0.3 ng/ml fluorescein equivalents; P < 0.001) than did non-contact lens wearers., Conclusions: Despite the known effects of long-term contact lens wear on corneal endothelial morphometry, no effect on endothelial function was found.

Purpose: To determine oxygen tension (PO2) on rabbit corneas beneath rigid gas permeable (RGP), hydrogel, and silicone elastomer lenses under open- and closed-eye conditions and to demonstrate the relationship between PO2 and overnight corneal swelling response in the rabbit model., Methods: An improved PO2 monitoring system (PO-2080) with a platinum-micro-wire-electrode was used to measure PO2. An ultrasonic pachymeter (DGH-2000) was used to measure corneal thickness after overnight wear., Results: The relationship between PO2 and oxygen transmissibility (Dk/ L) of the contact lens was linear for Dk/L between 0 and 70 x 10(-9) (cm/ sec)(mLO2/mL x mmHg). For Dk/L greater than 70 x 10(-9), PO2 gradually reached a plateau at 120 mmHg for open-eye conditions and 20 mmHg for closed-eye conditions. PO2 was inversely related to the overnight corneal swelling, ranging from 5.1% swelling at PO2 113.5/17.5 mmHg (open/closed-eye) for a hyper Dk/L lens (125 x 10(-9)) to 15.1% swelling at PO2 10.4/5.1 mmHg for a low Dk/L lens (11.5 x 10(-9))., Conclusions: Polarographic determination of PO2 provides reliable information about the amount of oxygen available to the cornea under a lens for both open-eye and closed-eye conditions. The data demonstrate that it is not possible to achieve normal oxygen levels with contact lens wear, even when hyper Dk/L lenses are worn.

After many years of successful contact lens wear, 3 long-term wearers of polymethyl methacrylate (PMMA) lenses (14, 15, and 18 years) and 1 long-term wearer of thick hydrogel lenses (11 years) suddenly developed intolerance to their lenses. Symptoms included ocular discomfort, reduced vision, and photophobia. All patients exhibited an excessive open-eye edema response with low to moderate Dk lenses. Posterior corneal changes included distortion of the endothelial mosaic and moderate to severe endothelial polymegethism. Patients were successfully refitted with lenses having higher oxygen transmissibility. It is proposed that long-term hypoxia and acidosis accompanying PMMA and thick hydrogel contact lens wear may be responsible for a syndrome characterized by endothelial dysfunction which results in inadequate regulation of corneal hydration and subsequent intolerance to contact lens wear. This condition has been termed Corneal Exhaustion Syndrome (CES).

Comfort, visual acuity, visual fields, daytime corneal edema and corneal staining were evaluated on 22 subjects wearing opaque tinted and non-opaque control hydrogel lenses. CooperVision Permaflex Mystique (38% polymacon) and Wesley-Jessen Durasoft 3 Colors (55% phemfilcon A) opaque lenses were compared to non-opaque lenses from the same manufacturers (CooperVision CV Classic and Wesley-Jessen Durasoft 3). Subjects were randomly assigned one type of opaque lens and one clear lens on each of two days, and two opaque lenses on another day. All lenses yielded similar results in terms of comfort, visual acuity, visual fields and corneal staining. The only visual problem with the opaque lenses was the reporting of "haziness" (usually peripheral) in 72 percent of Mystique and 59 percent of Durasoft 3 Colors trials. The greatest daytime corneal edema, 4.7 percent, occurred with the Mystique lens compared with 2.7 percent with CV Classic and 1.8 percent and 1.7 percent with the opaque and clear Durasoft 3 lenses respectively. These levels of edema were associated with a 40 percent incidence of striae with Mystique (17/43), 14 percent with the CV Classic (3/21 eyes), 5 percent with Durasoft 3 clear (1/22 eyes) and 2 percent with Durasoft 3 opaque lenses (1/44 eyes). Corneal swelling correlated with the measured Dk/L of the lenses. The Durasoft 3 Colors lens was the opaque tinted lens of choice based primarily on corneal physiology.

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.