Contact lens wear and the corneal endothelium

Contact lenses produce transient and permanent effects on the corneal endothelium in relationship to the lens oxygen transmissibility and how the contact lenses are worn. There is concern, as well as growing evidence, that contact lens-induced corneal endothelial pleomorphism causes a reduction in the endothelial functional capacity. This, in turn, may place an eye at risk for uncontrolled corneal swelling if the eye is under sufficient environmental or surgical stress. Use of lens materials and designs which promote high oxygen transmissibility, and patient wear of lenses during waking hours only, are ways to slow the development of permanent corneal endothelial pleomorphism.     

Contact lens intolerance induced by DM rupture and secondary endothelial degeneration. A specular microscopic study

Breaks or tears in the endothelium and Descemet's membrane (DM) are easily noticed in exact biomicroscopical ophthalmological examination. We present 2 patients with a large unilateral horizontal rupture in Descemet's membrane and abnormal corneal endothelia. In the area of the rupture the endothelial mosaic was highly abnormal, and there was no cell reflex. At the site of the rupture and at the periphery of the cornea of the affected eye the endothelial cell density was distinctly lowered, with pleomorphism and polymegathism. In an eye with a DM rupture and degenerated endothelium, difficulties in contact lens wear seem to be due to the hypoxia caused by soft contact lenses. For such patients, only gas-permeable hard lenses with short wearing times should be recommended. Check-ups should be frequent and meticulous. To ensure that endothelial degeneration is noticed well before corneal damage is clinically evident, the endothelial cells must be counted and changes sought for by specular microscopy.     

Corneal endothelial cell morphology under permanent wear of rigid contact lenses

The influence of the permanent wear of rigid high Dk-lenses (nominal Dk 71 or 92) with elliptical geometry on the corneal endothelium was assessed. For this purpose the endothelium of 16 patients was compared by specular microscopy before and after the permanent wear. The wearing time of the lenses varied between 7 and 24 months. Computerized morphometric analysis of the photographs revealed that the variability in cell size (polymegathism) and in cell shape (pleomorphism) did not change during the wearing period. It is suggested that this is due to the high gas-permeability and the elliptical geometry of the contact lenses.     

CORNEAL ENDOTHELIAL CHANGES IN SUPERFICIAL EPITHELIAL KERATOPATHY

A series of five cases is described in which superficial punctate keratopathy was associated with endothelial cell changes. The most striking change was the presence of dark areas or blebs, usually two to four cell diameters in extent. There was also distortion and crumpling of the corneal endothelium, mild pleomorphism and polymegathism of the endothelial cells, with a reduced cell count in some cases. These blebs have previously been reported in hard and soft contact lens wearers and are due to intercellular oedema with separation of endothelial cells from Descemet's membrane. Anoxia and interference with osmosis have been proposed as possible mechanisms for the production of these blebs, but our cases demonstrate that fine disruption of the corneal epithelium can affect the integrity of the corneal endothelium and may lead to significant damage over a Ion period of time.     

Corneal endothelial changes in superficial epithelial keratopathy

A series of five cases is described in which superficial punctate keratopathy was associated with endothelial cell changes. The most striking change was the presence of dark areas or blebs, usually two to four cell diameters in extent. There was also distortion and crumpling of the corneal endothelium, mild pleomorphism and polymegathism of the endothelial cells, with a reduced cell count in some cases. These blebs have previously been reported in hard and soft contact lens wearers and are due to intercellular oedema with separation of endothelial cells from Descemet's membrane. Anoxia and interference with osmosis have been proposed as possible mechanisms for the production of these blebs, but our cases demonstrate that fine disruption of the corneal epithelium can affect the integrity of the corneal endothelium and may lead to significant damage over a long period of time.     

长期配戴角膜塑形镜对角膜厚度和角膜内皮细胞的影响

目的评价近视眼患者长期配戴角膜塑形镜对角膜厚度和角膜内皮细胞的影响。方法利用超声角膜测厚仪和非接触角膜内皮显微镜,测量和观察132名青少年近视眼患者（264只眼）配戴角膜塑形镜（透氧系数为100）前和戴镜期间的角膜中央和旁周边部的角膜厚度,以及角膜内皮细胞的密度和形态学改变。结果无论采用夜戴方式还是日戴方式配戴角膜塑形镜3年以上,角膜中央及旁周边部厚度均无明显改变（P〉0．05）,角膜内皮细胞密度均无明显降低（P〉0．05）,角膜内皮细胞平均面积和细胞变异系数均无明显增大（P〉0．05）,角膜内皮细胞六角形比率均无明显降低（P〉0．05）。结论利用高透氧材料的角膜塑形镜进行科学的角膜塑形治疗,对角膜代谢的影响轻微,长期配戴用于控制近视发展基本是安全的。     

Deep corneal stromal opacities with contact lenses

Two patients with deep corneal stromal opacities occurring after prolonged contact lens wear are described. The opacities were associated with folds or striae in Descemet's membrane which they overlay. Development of the opacities was associated with ocular discomfort, photophobia, reduced vision and a history of prolonged daily wearing times. Although the corneal endothelial cell counts were within the normal range, the count was reduced in the affected eye in the patient with the unilateral deep stromal opacity and there was mild polymegathism of the endothelial cells. It is possible that the long-term effects of subtle endothelial cell changes may cause a keratopathy with later scarring and opacification. Poor oxygen transmissibility, carbon dioxide build-up, or suction effects by the lens may all be aetiological factors. Early recognition and treatment, particularly with a better fitting lens of high oxygen transmissibility is important, as once developed the opacities regress only slowly and may result in permanent visual impairment.     

DEEP CORNEAL STROMAL OPACITIES WITH CONTACT LENSES

Two patients with deep corneal stromal opacities occurring after prolonged contact lens wear are described. The opacities were associated with folds or striae in Descemet's membrane which they overlay. Development of the opacities was associated with ocular discomfort, photophobia, reduced vision and a history of prolonged daily wearing times. Although the corneal endothelial cell counts were within the normal range, the count was reduced in the affected eye in the patient with the unilateral deep stromal opacity and there was mild polymegathism of the endothelial cells. It is possible that the long-term effects of subtle endothelial cell changes may cause a keratopathy with later scarring and opacification. Poor oxygen trans-missibility, carbon dioxide build-up, or suction effects by the lens may all be aetiological factors. Early recognition and treatment, particularly with a better fitting lens of high oxygen transmissibility is important, as once developed the opacities regress only slowly and may result in permanent visual impairment.     

Corneal endothelial polymegathism after the extended wear of rigid gas-permeable contact lenses

To determine if there are any corneal endothelial cell size and shape changes in subjects wearing rigid gas-permeable contact lenses for cosmetic extended wear, six unadapted lens wearers were fitted using four different lens materials. Each subject wore one lens extended-wear and the other daily-wear for 3 months. Before lens wear and after 3 months, noncontact endothelial photographs were taken. Cell tracings were analyzed by a digitizing computer. This study showed significant endothelial polymegathism, an increase in maximum cell area to minimum cell area, and a significant decrease in percent frequency of hexagonal cells in the extended-wear eyes. There existed in these subjects a significant correlation between changes in cell size (polymegathism) and cell shape (pleomorphism).     

Analysis of the corneal endothelium in keratoconus

The corneal endothelium in nine cases of keratoconus (18 eyes) was analyzed quantitatively for mean cell area and standard deviation (SD) of cell area to determine the presence of polymegathism. Four of the subjects were veteran wearers of rigid contact lenses and five of the subjects had not worn contact lenses previously. The subjects were matched for age, sex, and contact lens history with a group of normals. The endothelium in eyes with keratoconus did not show a significant increase in the extent of polymegathism as compared with controls. There was no significant difference in mean cell area between the study group and the control group. These results suggest that polymegathism in keratoconic patients may be related to contact lens wear.     

Effects of long-term extended contact lens wear on the human cornea

The effects of long-term extended wear of soft contact lenses on the human cornea were determined by examining 27 patients who had worn a high water content hydrogel contact lens in 1 eye only for an average of 62 +/- 29 months (mean +/- SD). The other eye, which was either emmetropic or amblyopic, acted as a control. The lens-wearing eye showed a 14.8% reduction in epithelial oxygen uptake (P less than 0.001), a 5.6% reduction in epithelial thickness (P less than 0.05), a 2.3% reduction in stromal thickness (P less than 0.05), the induction of epithelial microcysts, and a 22.0% increase in endothelial polymegathism (P less than 0.001). Endothelial cell density was unaffected by extended lens wear. No interocular differences in any of these physiological characteristics were found in a matched control group of anisometropic and amblyopic subjects who did not wear contact lenses. The patients ceased lens wear for up to one month and recovery of corneal function was monitored during this period. Epithelial oxygen uptake and thickness recovered within 33 days of lens removal. The number of microcysts increased over the first 7 days, but decreased thereafter; some microcysts were still present 33 days after lens removal. Recovery from stromal thinning had not occurred after 33 days following lens removal. There was a slight reduction in polymegathism in some patients, but overall this was not statistically significant. These findings establish (1) that the extended wear of hydrogel lenses induces significant changes in all layers of the cornea; (2) that lens wear suppresses aerobic epithelial metabolism, which may compromise the epithelial barrier to infection; and (3) that changes to the stroma and endothelium are long-lasting. Lens-induced effects on corneal physiology can be minimized by fitting lenses that have greater oxygen transmissibility (are thinner), are more mobile, more frequently removed, and more regularly replaced.     

A morphologic and fluorophotometric analysis of the corneal endothelium in long-term extended wear soft contact lens wearers

Eleven extended wear soft contact lens wearers with an average of 4 years of wear underwent corneal fluorophotometry and quantitative specular microscopy. Compared to age-matched controls, a significant increase in mean endothelial permeability was found in the contact lens group, indicating a defect in their endothelial barrier function. A significant increase in the mean endothelial pump rate was also noted in the contact lens group. In addition, mean corneal thickness was significantly greater in the contact lens group. No significant difference was noted between the two groups in mean cell area and figure coefficient; however, the coefficient of variation was significantly higher in the contact lens group. Duration of contact lens wear correlated positively with coefficient of variation. An inverse correlation was noted between contact lens oxygen transmissibility and cell area, as well as corneal thickness. These data suggest both a morphologic and functional defect in the corneal endothelium of long-term extended wear soft contact lens wearers.     

The effect of long-term contact lens wear on the cells of the cornea.

PURPOSE: To review the effects of long-term contact lens wear on the cells of the cornea. METHODS: Published investigations into the effects of long-term contact lens wear on the corneal epithelium, keratocytes, and endothelium were reviewed. RESULTS: Results from multiple studies indicate that long-term daily wear of contact lenses causes endothelial polymegethism but has no effect on corneal epithelium (thickness, surface cell size); keratocytes (density, stromal reflectivity); or endothelial cell density, permeability, or pump rate. Extended wear also causes no endothelial changes other than polymegethism, but it affects the epithelium (decreased thickness, increased surface cell size) and keratocytes (possible decreased density). CONCLUSIONS: Investigators have not found detrimental effects on the cells of the cornea from the long-term use of daily wear contact lenses. Although contact lenses cause endothelial polymegethism, no functional deficits ensue. Extended wear lenses may cause changes in all three cell types, but it is not known if these effects are detrimental nor if they occur with newer lenses of higher oxygen transmissibility. Patients can be reassured that modern contact lenses can be worn for many years in daily wear fashion (and possibly in extended wear with lenses of very high oxygen transmissibility) without damaging the cells of the cornea.     

Physiologic changes of the cornea with contact lens wear.

PURPOSE: This article reviews the corneal changes resulting from the hypoxia that occurs during sleep and specifically during contact lens wear. METHODS: Discussion includes a literature review and observations regarding the changes to the corneal epithelium, stroma, and endothelium that take place during sleep and wearing of contact lenses made from different materials. RESULTS: Hypoxia and hypercapnia cause significant changes to the corneal epithelium, stroma, and endothelium. Some of these changes can also be seen following the sleep cycle. Epithelial changes include decreased metabolic rate, morphologic changes, microcysts, changes in junctional integrity, decreased corneal sensation, and pannus formation. Stromal changes include stromal edema, stromal acidosis, neovascularization, and changes in corneal shape and, ultimately, corneal thinning. Endothelial changes include bleb formation, polymegethism, changes in endothelial cell density, and possible changes in endothelial function. CONCLUSIONS: There are multiple and significant corneal changes resulting from hypoxia and hypercapnia. These changes vary with the specific lens style. The high-oxygen-permeable contact lenses recently introduced may overcome some of these problems.     

Diurnal Variation in Corneal Endothelial Morphologyp

Transient changes in the corneal endothelium were the earliest detectable response to low atmospheric oxygen in experimental animals. Similar changes have been reported after hard and soft contact lens wear. We describe widespread transient cell changes by wide-field specular microscopy in the normal corneal endothelium after 12 hours of a light eye patch. The relative anoxia of lid closure during normal sleep appears to be the cause of observable changes. This observation questions the safety of extended wear contact lens over a prolonged period of time, and its significance to age-related endothelial cell density reduction and cornea guttata remains to be seen.     

Effects of contact lens-induced hypoxia on the physiology of the corneal endothelium.

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.     

Hypoxic effects on corneal morphology and function

Normal corneal metabolism depends on a critical level of oxygen, below which a series of acute corneal responses occur, including an increase in stromal lactate, a reduction in intercellular pH, and an increase in corneal hydration. These acute responses are reversible when normal oxygen is restored; however, it has been shown that chronic exposure to low oxygen levels can result in permanent morphologic changes in the corneal endothelium. Clinicians have expressed concern that these observed structural changes may also be accompanied by alterations in corneal physiology. Whether such effects occur is not known, since it has been difficult to assess human corneal function accurately. Recently, we have developed an in vivo test, able to measure overall corneal hydration control, that can be used to study the effects of hypoxia on corneal function. This test provides information on several characteristics of hydration control, one of which is the percent corneal thickness recovery per hour (PRPH) after inducing corneal swelling. In this study, we assumed that corneal hypoxia accompanies both extended and polymethylmethacrylate (PMMA) contact lens wear and that the dose received is related to the years of past lens wear. Using this paradigm, we explored the relationship of hypoxic dose to an endothelial polymegethism index (EPI), endothelial cell density (ECD), and PRPH in 36 subjects with varying contact lens wearing histories. Based on multiple regression analysis, the relative change (expressed as percent per year) associated with hypoxic dose (adjusted for age and gender) was found to be dose-dependent and corresponded to estimated changes of 1.70%/yr, -0.25%/yr, and -1.26%/yr, with 95% confidence limits of (-0.3, 3.7), (-1.4, 0.9), and (-2.6, 0.06) for EPI, ECD, and PRPH, respectively. These preliminary data suggest that hypoxic exposure alters endothelial morphology and reduces corneal function; however, it is important to indicate that this was a exploratory investigation with several limitations, and that therefore these results should be viewed as preliminary until more definitive studies are completed.     

Evaluation of endothelial integrity in extended wear

The purpose of this investigation was two-fold: 1) to evaluate and compare the endothelium of hydrogel and rigid extended wear contact lens patients and 2) to evaluate a new technique for in-office endothelial photography. Endothelial photography was performed on seven patients who had worn low water content ultrathin soft lenses and seven patients who had worn rigid extended wear lenses for 1 year. In addition, seven non-lens wearers were used as a control group. Endothelial polymegathism and pleomorphic changes were evaluated via photographic observation using a new endothelial photography technique developed by G. Michael Murphy, O.D. The results showed that this was a viable method of endothelial photography for monitoring extended wear contact lens patients.     

Diabetes and contact lens wear

The literature suggests that diabetic patients may have altered tear chemistry and tear secretion as well as structural and functional changes to the corneal epithelium, endothelium and nerves. These factors, together with a reported increased incidence of corneal infection, suggest that diabetic patients may be particularly susceptible to developing ocular complications during contact lens wear. Reports of contact lens-induced complications in diabetic patients do exist, although a number of these reports concern patients with advanced diabetic eye disease using lenses on an extended wear basis. Over the past decade or so, there have been published studies documenting the response of the diabetic eye to more modern contact lens modalities. The results of these studies suggest that contact lenses can be a viable mode of refractive correction for diabetic patients. Furthermore, new research suggests that the measurement of tear glucose concentration could, in future, be used to monitor metabolic control non-invasively in diabetic patients. This could be carried out using contact lenses manufactured from hydrogel polymers embedded with glucose-sensing agents or nanoscale digital electronic technology. The purpose of this paper is to review the literature on the anterior ocular manifestations of diabetes, particularly that pertaining to contact lens wear.     

Discoveries in research on diabetic keratopathy.

BACKGROUND: Researchers exploring the mechanisms of diabetic changes in numerous body tissues have evidence that the complications may result from the consequences of increased aldose reductase activity. Aldose reductase is the rate-limiting enzyme in the polyol pathway in which glucose is converted to sorbitol. METHOD: Sorbitol accumulation from increased aldose reductase activity may play a role in diabetic corneal pathology as well. Studies of animals involving diabetic models have shown both structural (polymegathism, pleomorphism) and functional (increased permeability, slower recovery from induced edema) changes in the diabetic corneal epithelium and endothelium. Some studies of human beings have confirmed these findings. However, differences in the groups of human subjects between studies (such as age, type of diabetes, state of glycemia. duration of disease, etc.) may account for the sometimes conflicting results. RESULTS: Treatment with aldose reductase inhibitors has been shown both to reduce corneal changes after they have occurred and to limit the development of these corneal changes when compared to untreated controls in both animals and human beings. CONCLUSION: The mechanism by which increased aldose reductase activity contributes to diabetic corneal pathology remains unknown.