Practitioners should be mindful of all of the variables that can lead to corneal edema.

There’s no doubt that modern eyecare has embraced the rebirth of scleral lenses. Scleral GP contact lenses are the fastest growing segment of the GP market.1 Lens material manufacturers are providing large-diameter, high-Dk lens buttons. In addition, lens manufacturers are introducing designs to enhance fitting success and to improve patient outcomes. Online fitting tools are available for practitioners to modify lens designs, providing better control of the scleral lens vault over the cornea and limbus and for better lens alignment over the asymmetric sclera. New technology is available to more accurately measure scleral shape, allowing for a more accurate lens design and fit. The number of practitioners mastering scleral lens fitting skills continues to increase.

The use of scleral lenses to treat complex corneal diseases (i.e., irregular corneas and/or ocular surface disease) also continues to grow. More and more practitioners are realizing the benefits that these lenses can offer with regard to visual rehabilitation and ocular surface function restoration. These lenses offer great benefits that can translate into patient comfort; great best-corrected visual acuity (BCVA); ocular surface protection from the environment of the lids, desiccation, and/or chronic exposure; and even corneal remodeling. However, complications can also arise.

To be better equipped to manage complications that may arise secondary to—or during—scleral lens wear, it is critical to understand the disease etiology being treated and the underlying factors that can lead to these complications. For example, one complication that can arise that is often discussed but not necessarily well understood is corneal edema.

In this article, we will review and discuss the causes and treatment options for corneal edema in the setting of scleral lens wear.


Clinical corneal edema can arise secondary to congenital, degenerative, traumatic, or inflammatory processes as well as to changes in intraocular pressure (IOP).2 At a pathophysiological level, it can be due to some malfunction in the endothelium, an increase in IOP, or a combination of both.2,3

In the context of scleral lens wear, several factors should also be ruled out when observing corneal edema during scleral lens wear: a) hypoxia, which, in turn, is affected by the oxygen permeability of the lens material; b) increase in IOP; c) functional condition of the endothelium; and d) the presence of negative pressure (suction) under a scleral lens.4

Hypoxia The corneal epithelium receives most of the oxygen required for normal metabolism from atmospheric oxygen that dissolves in the tear layer. Historically, contact lenses were first made with glass and then PMMA plastic, materials that are impermeable to oxygen. These early scleral lenses could be worn for just a few hours before oxygen deprivation problems developed. For instance, Sattler’s veil (a.k.a. Fick’s phenomenon) is a clouding of the corneal epithelium due to an insufficient supply of oxygen caused by the oxygen-impermeable contact lens creating a barrier to the acquisition of oxygen.5 With removal of these early scleral lenses, the corneal clouding quickly resolved.

In 1996, Chahine and Weissman reported that the use of low-Dk hydrogel contact lenses caused superficial limbal corneal vascularization, furrow staining, limbal epithelial hypertrophy, and conjunctival hyperemia.6 When silicone hydrogel contact lenses became available in 2002, changing from low-Dk hydrogel lenses to silicone hydrogel lenses resolved the occurrence of these problems in soft contact lens daily wear. Mild bulbar injection resolved, and both furrow staining and limbal epithelial hypertrophy disappeared. Resolution of these problems was attributed to the use of higher-oxygen-permeable soft lenses, with Dk values greater than 100. Until this report was published, these subtle corneal changes were either unnoticed or ignored by contact lens fitters, or practitioners did not recognize them as being abnormal.

Recently, there has been much discussion and articles written about clinical studies that address the role of oxygen tension and of post-lens tear layer thickness, polymer material Dk/t, effects on corneal metabolism, and how those correlate with hypoxia-related complications and corneal edema during scleral lens wear.7-13 There is a theoretical model stating that the post-lens tear layer thickness should be less than 150μm to avoid hypoxic effects on the cornea.13 However, most clinical studies report amounts of corneal edema that are within the range of physiological edema that occurs during sleep (4%), and, in most cases, this amount is less than 2%, despite post-lens tear layer thicknesses being greater than 250μm.7-11

One recent study showed that increasing post-lens tear layer thicknesses has minimal impact on the range of corneal edema observed with scleral lens wear. The measured amounts of corneal edema (1% to 1.5%) were also less compared to the physiological levels that occur overnight with lid closure during sleep (4%).7 This study looked at two variables and their effect or impact on corneal edema during lens wear: post-lens tear layer thickness and polymer Dk/l (Dk/t) values. Based on their findings, emphasis should be given to Dk/l values to prevent hypoxia-related complications, versus post-lens tear layer thickness values.7

Vincent et al also observed no clinically significant edema after eight hours of mini-scleral lens wear with a median central clearance of ~350μm.8 Their findings suggest that the amount of central clearance or post-lens tear layer thickness does not contribute significantly to corneal hypoxia—in the wearing schedule studied—in healthy subjects.

These recent findings also support previous clinical observations, showing that, despite resulting lens clearances of more than 150μm, scleral lenses provide ocular surface restorative functions, for example in the setting of healing persistent epithelial defects in compromised corneas,14,15 in corneal remodeling, neovascularization regression, clearing of corneal opacities (Figure 1),16-18 and in the management of dry eye patients.19 These recent studies highlighting the role of Dk/t value of the lens also seem to support Chahine and Weissman’s report on hypoxia-related complications with soft lenses.6

Figure 1. A case showcasing complete corneal remodeling and improvement at the cornea—at initial presentation (A); after two months (B); after two years of scleral lens wear (C); and with a central clearance of ~≥450μm and no signs of clinically significant edema (subjective or objective) (18.5mm scleral lens/material Dk 85) (D). With a center thickness (CT) of 200μm, the Dk/l of the system was ~40, which, based on Kim et al,6 is more than an adequate Dk/l value to prevent clinically significant edema and may explain the dramatic clinical benefits in this case.
Images reprinted with permission from J Ophthalmol Clin Res.17

Increased IOP As practitioners expand their use of scleral lenses beyond visual rehabilitation for irregular corneas and use them to treat ocular surface disease, it is extremely important to realize and understand that hypoxia may not be the only cause for corneal edema during scleral lens wear.

Ytteborg and Dohlman reported in 1965 that corneal epithelial edema appears sooner and progresses more rapidly as the level of IOP increases.20,21 These findings were later supported by other studies in which the researchers found that endothelial cells are compromised by increased IOP and that a decrease in endothelial cell density and damage to the active pump system secondary to morphological damage are responsible for the resultant epithelial corneal edema.22,23

Could the endothelial function be compromised at baseline as part of the disease etiology (e.g., failing graft, pseudophakic bullous keratopathy [PBK], Fuchs’ dystrophy)? If there is a compromised endothelium and corneal edema is observed at baseline, it will only get worse during scleral lens wear; that patient may simply not be a good candidate for scleral lenses. Are there any concomitant diseases (e.g., glaucoma)? Is the patient taking topical steroids? Are steroids managed properly and risk for steroid response properly monitored? Could suction or negative pressure behind the scleral lens haptic play a role?

Therefore, whenever epithelial corneal edema is observed—aside from a careful evaluation of the lens fit (more on this below) to determine whether there is adequate alignment, no lens suction from a very tight lens or crowding at the limbal region, an adequate Dk/t in the lens system, and/or tear exchange—it is imperative to always check the IOP; all that may be needed is to properly manage and lower the IOP (Figure 2).

Figure 2. Manifestation of microcystic epithelial corneal edema and reduced BCVA after an acute increase in IOP. BCVA went down from 20/25 to 20/50. IOP went up from a range of 17 mmHg to 32 mmHg. This patient has neurotrophic keratopathy and glaucoma and had been a successful scleral lens patient for five years, with the goal to support the ocular surface. Corneal edema resolved once the IOP in the left eye was properly managed. There was no need to revise the fit.
Image courtesy of Karen G. Carrasquillo, OD, PhD

This is especially relevant if the patient also suffers from glaucoma or if the patient is currently taking topical steroids, because there might be a steroid response. Consider a scenario in which IOP increases and the practitioner fails to check it, instead solely focusing on hypoxia and lens troubleshooting. Not only will it take much longer for the practitioner to resolve the issue, but this will also result in poor patient management and the possibility of further complications.

Lens Suction Miller, Carroll, and Ridley were some of the first to report on the effects of scleral lens suction (cling) and the development of corneal epithelial edema.4,24 They defined cling, or suction, as the force necessary to pull a lens from the eye. They reported that when this force is created as a result of prolonged contact between the lens and the globe, it is further enhanced by factors such as swelling of the conjunctiva and the force exerted by the lids with blinking.4 When these forces are all operating, it seems that there’s enough force to further enhance the accumulation of fluid within the corneal epithelium. Even when these concepts were first introduced during the scleral lens PMMA era, there was an idea of a fluid-ventilated scleral lens (including the design of channels under the scleral lens haptic), not only to maximize tear exchange under the lens, but also to prevent/minimize lens suction.25 This phenomenon still occurs with GP lens materials.

In our clinic, we have witnessed numerous cases (Figures 3, 4, and 5) in which, after addressing a tight lens fit or significant crowding at the limbal area, either limbal edema or corneal edema resolves. Troubleshooting often includes increasing the lens diameter, ensuring adequate limbal clearance, and adding channels under the scleral lens haptic. Therefore, ruling out scleral lens suction should also be part of the troubleshooting strategy when noticing/observing corneal edema.

Figure 3. Limbal edema as a result of crowding/touch along the limbal region—contributing to lens suction and difficult removal (A). Edema was resolved (B) after increasing the limbal clearance (C).
Image courtesy of Karen G. Carrasquillo, OD, PhD

Figure 4. Diffuse epithelial corneal edema as a result of crowding/touch along the limbal region and a tight-fitting lens—contributing to lens suction and difficult removal (A). Edema was resolved (B) after increasing the limbal clearance and flattening/loosening the haptic (C).
Image courtesy of Karen G. Carrasquillo, OD, PhD

Figure 5. Increased neovascularization and edema along the graft-host junction in a post-PK cornea secondary to Fuchs’ dystrophy (A). The material was Boston XO2 (Dk 141) (Bausch + Lomb) with CT of 250μm at the time. Edema and neovascularization resolved after adding channels under the haptic surface at 3 o’clock and 9 o’clock to prevent/minimize suction (B). An example of channels added in four meridians—such as the ones added in the case above and in similar cases to promote tear exchange and minimize/prevent suction (C).
Image courtesy of Karen G. Carrasquillo, OD, PhD


In general, techniques such as sclerotic scatter and retroillumination are great ways to detect epithelial corneal edema. In sclerotic scatter, if a white light beam of medium width is focused obliquely at the temporal limbus, the diffraction of light from the area of edema will appear as a slight corneal haze. The sensitivity of this technique is enhanced by studying the contrast of light scatter at the junction between the normal and edematous cornea against the background of the black pupil.25 With retroillumination, it is possible to see the presence of fine micro bullae or the presence of epithelial microcysts (Figure 6).

Figure 6. Microcystic epithelial edema (MCE) as seen by retroillumination.
Image courtesy of Karen G. Carrasquillo, OD, PhD

Another way to detect edema is by noting the presence of negative staining over the cornea when stained with sodium fluorescein (Figure 7). Decreased BCVA, steepening in corneal curvature, and increase in corneal thickness are other objective measures that can be used to corroborate and confirm the diagnosis.4

Figure 7. Microcystic epithelial edema (MCE) as seen by the presence of negative staining when stained with sodium fluorescein.
Image courtesy of Karen G. Carrasquillo, OD, PhD

A timely and thorough slit lamp examination is important. With the scleral lens still in place, use a 1mm to 2mm band of white light to carefully examine the limbal area using direct and indirect retroillumination. Examine the limbal vascular arcade for areas of micro-pannus or fronds neovascularization (Figure 8).

Figure 8. Vascularization along the superior limbus. The lens material has a Dk of 141, a lens thickness over the limbus of 0.35mm, and a tear lens thickness of 30 microns.
Image courtesy of Steve Byrnes, OD.

Re-examine the limbus and peripheral cornea immediately upon removal of the scleral lens. Furrow staining and limbal epithelial hypertrophy are very difficult to see with white light. Instilling sodium fluorescein into the tear layer enhances surface irregularities. With low-to-medium slit lamp magnification, illuminate the area being observed with a broad band of cobalt blue light using moderate-to-high light intensity. Place a yellow barrier filter over the slit lamp objective lens to further enhance the differences in the fluorescein layer and to discover subtle areas of epithelial staining and pooling. Have the patient blink and then observe the tear layer dissipate from the surface. As the tear layer thins, pools of fluorescein highlight areas adjacent to swollen epithelium (Figure 9). If limbal microcysts are present, they also will be highlighted, and areas of positive and negative staining may be present (Figure 10).

Figure 9. Furrow staining (pooling of fluorescein-saturated tears) and limbal epithelial hypertrophy immediately after lens removal.
Image courtesy of Steve Byrnes, OD.

Figure 10. Limbal microcysts noted immediately after lens removal. The patient was wearing a 14.3mm diameter, –8.25D, +2.50D add multifocal scleral lens with a midperipheral thickness of 0.45mm and a limbal clearance of 20 microns. Conjunctival impingement staining is also present.
Image courtesy of Steve Byrnes, OD.

Observe the overall corneal surface. It should be smooth and regular. Undulations in the surface and swollen areas of epithelium will create a mottled mosaic pattern in the fluorescein-enhanced tear layer. Oxygen deprivation effects are a cumulative problem. Examine the limbal areas covered by the upper and lower eyelids. Eyelid coverage decreases the available oxygen to these areas.

Patients may occasionally forget to remove lenses before bedtime and admit to napping while wearing their lenses. Corneal edema from closed-eye lens wear (Figure 11) is best observed as soon after awakening as possible. With exposure to atmospheric oxygen in open-eye conditions, the corneal edema will begin to resolve. If a compliant daily wear patient is being examined, schedule the patient at close to the end of the wearing time, or as late in the day as scheduling permits, so that the cumulative effect of oxygen deficit from daily wear for that patient can be observed. For patients who admit to sleeping in their lenses, schedule follow-up appointments as early in the day as scheduling permits.

Figure 11. Corneal edema after accidentally wearing a scleral lens overnight. Note the furrow staining in the periphery and epithelial blebs and microcysts scattered throughout the cornea.
Image courtesy of Karen G. Carrasquillo, OD, PhD

The possibility of forgetting to remove the lenses before sleep is high. So, what happens when these lenses are worn overnight in the closed-eye condition? Patients may awaken to Sattler’s veil, corneal clouding, haloes around lights (Figure 12), and sensitivity to light. Interestingly, these symptoms and signs start to resolve immediately upon opening the eyes, as a percentage of atmospheric oxygen becomes available through the plastic of the scleral lens. If the patient is not scheduled to be seen when this problem occurs, the practitioner may never see it.

Figure 12. Our view in (A) when there is microcystic epithelial edema and the patient’s view out (B).
Image courtesy of Steve Byrnes, OD.

In general, as far as subjective measures go, patients, upon questioning, will report hazy and/or decreased vision with increased lens wear time and will report the presence of concentric rainbow rings around light sources reminiscent of Sattler’s veil (Figure 12). They may also report increased glare sensitivity.


As practitioners, what can we do to minimize scleral lens complications secondary to corneal edema? Obviously, a proper fit is important. The lens design is important. The contact lens power, optic zone diameter, midperipheral lens design, base curve, and peripheral zone design all contribute to the oxygen transmission to the corneal surface.

While lens material manufacturers provide the lens power, diameter, base curve, and sometimes center thickness of the lens, they do not provide a thickness profile of the lens specifying the Dk/t at various points along that profile. To capture this information, practitioners can use a thickness gauge to measure the center thickness, the lens thickness at the edge of the optic zone, the midperipheral zone thickness, and the peripheral zone thickness; that information will help them better understand the oxygen transmission possibilities of the lens design being used. If oxygen deprivation problems arise, practitioners can work with the lens manufacturer to modify the lens design and/or to change the lens material. Thinner lenses made of higher-Dk lens materials than what are currently available may still be needed to achieve the oxygen transmission levels that current high-Dk silicone hydrogel soft lenses have achieved.

More studies, especially long-term studies, are needed to answer many questions related to this topic. For example, what’s the long-term impact, if any, of physiological edema levels with prolonged scleral lens wear? What’s the role of lens diameter (most clinical studies use mini-scleral lens designs) in corneal edema findings? Could other factors play a role (i.e., amount of tear exchange)? Does lens suction play a more significant role? If so, does lens diameter have a role in minimizing the amount of negative pressure (suction) under a scleral lens? Or is the negative pressure built under a scleral lens strictly related to tight-fitting lenses? Or could it be that perhaps a fine balance among all of the factors mentioned above is required?

Until we find the answers to these and other questions, continuing to be mindful of all of the variables that can lead to corneal edema in the context of scleral lens wear, while never forgetting to see the big picture in each case, will allow us to better manage and care for our patients. CLS


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