Modifications to lens material, design, and wearing time can help reduce the risk of hypoxia with scleral lens wear.

Modern scleral lenses are an amazing, potentially life-changing technology. The growth in the scleral lens market and in the number of speciality contact lens practitioners in recent years1 demonstrates their utility in the therapeutic treatment of ocular surface disease, the visual restoration of the irregular cornea, and the correction of simple refractive errors in patients who have normal corneas.2

However, our understanding of scleral lenses has continued to evolve over the past decade, and the approach to lens fitting is continually revisited. While much remains unknown, it is clear that scleral lenses can generate their own unique challenges and complications,3 and they simply may not be the most appropriate contact lens modality for some patients. For example, in keratoconus patients, visual acuity may be suboptimal with scleral lenses due to higher-order aberrations associated with lens decentration compared to traditional smaller GP or hybrid lenses.4 In post-graft patients (PK), a low endothelial cell count—or more precisely, a lower number of healthy endothelial cells—may be considered a potential contraindication to scleral lens wear.5 In such cases, smaller GP lenses may provide a healthier option, albeit perhaps a more challenging fit.

This brings us to the debate concerning oxygen delivery to the cornea through scleral lenses. This article aims to summarize recent findings from both theoretical modeling and in vivo studies, and it advocates for a measured approach when fitting scleral lenses by considering the risks and benefits for each patient.


A theoretical model based on the Harvitt-Bonanno criteria was first developed in 20126 and was soon followed by another model using a mathematical approach.7 Both models suggested that scleral lenses may generate hypoxia-related stress to the central cornea if the lens material has limited oxygen permeability and if the lens is designed such that it has increased thickness and results in increased tear fluid reservoir thickness. Consequently, both authors recommended that scleral lenses should be manufactured in high-oxygen-permeable materials (Dk greater than 150), with a maximum thickness of 250 microns and fitted with a central tear reservoir of 200 microns or less.

These models were not challenged on their exactitude or scientific value, but questions were raised about their clinical significance,8 especially in light of the favorable outcomes regularly encountered in clinical practice under adverse conditions.9,10 Some of these authors suggested that in the absence of obvious clinical signs, any hypoxia-related ocular sequelae would be minimal; however, clinical studies were needed to determine the right approach.


To evaluate the presence and the clinical impact of hypoxia-related stress on the cornea, it is important to base our analysis on well-controlled experiments rather than on case reports or case series.

More recent studies provided evidence that scleral lens wear was associated with hypoxia-related stress, manifesting as 1% to 3% corneal edema in young healthy eyes, depending on the lens design, material, and fitting protocol. Most of the authors of these studies considered this level of hypoxia as benign,11-14 comparable to the magnitude of edema observed following overnight eyelid closure or following daily wear of some soft hydrogel lenses, with no significant short-term side effects.

This comparison can be misleading. Despite a similar level of corneal swelling, physiological edema typically resolves within one hour of eyelid opening as a result of exposure of the cornea to atmospheric oxygen. Hypoxia-related stress secondary to scleral lens wear occurs rapidly, within the first 45 minutes,15 and persists for all wearing hours. Consequently, if scleral lenses are applied shortly after waking, the cornea may theoretically be under constant hypoxia-related stress. Currently, no studies have investigated the longer-term effects of low-grade scleral lens-induced corneal edema on corneal health and visual outcomes.


One of the first in vitro studies examining scleral lens wear and hypoxia revealed that oxygen delivery to the cornea is reduced by 30% at the epithelial level for a 400-micron tear reservoir compared to the recommended reservoir of 200 microns.16 This clinical study validated previous theoretical models and was supported by other clinical work demonstrating that stromal edema increased slightly with a thicker tear reservoir (an estimated 25% reduction in oxygen for a 431-micron reservoir compared to a 225-micron reservoir).15 In this study, the onset of stromal edema was rapid and diminished slightly with wearing time, but never fully recovered over eight hours of lens wear. Based on these findings, the authors advocated for a minimal-clearance approach to reduce potential hypoxia-related stress, particularly for compromised corneas (low endothelial cell count).16

More recently, another clinical in vivo study demonstrated a significant endothelial response to hypoxia-related stress associated with scleral lens wear.17 Blebs, a rapid-onset consequence of corneal hypoxia and acidosis18 that are transient in nature, were identified shortly after lens application and were more numerous in lenses fitted with an increased reservoir thickness (400 microns compared to 200 microns). When this physiological response was first identified in soft lens wearers in the late 1970s,19 it galvanized the entire contact lens industry to develop new materials that provided more oxygen to the cornea. Can we expect the same reaction from researchers and manufacturers based on this new finding?

In the meantime, these clinical studies confirm that a hypoxia-related response to scleral lens wear may be observed in multiple corneal layers, particularly when scleral lenses are fitted with an increased tear reservoir.


Tear exchange and tear mixing during scleral lens wear have been suggested as potential alternative sources of oxygen delivery to the cornea. However, recent studies examining scleral lens tear exchange suggest that following lens settling, there is minimal tear exchange (less than 0.5% per minute) that is substantially less compared to that with soft lenses (~6% per minute).20,21 Consequently, tear exchange cannot be considered a viable mechanism to alleviate hypoxia-related stress during scleral lens wear, particularly if the peripheral curves are aligned, quadrant by quadrant, to the underlying conjunctival and scleral tissue, which increases the potential for seal-off.

In contrast, tear mixing is based on the principle that, upon blinking or eye movements, a scleral lens moves on the conjunctiva and generates fluid displacement within the reservoir. More posterior fluid closer to the cornea can then circulate anteriorly to the posterior lens surface where, in theory, it may be replenished with atmospheric oxygen. Tear mixing with scleral lenses does appear to be limited,22 and if present, it may be enhanced if lenses are fitted with a thinner tear reservoir.

Some scleral lenses can be adapted to increase tear exchange if designed with channeled peripheral curves23 or with loose peripheral curves. Both strategies may enhance tear exchange and provide a renewable source of oxygen to the cornea despite an increased lens and reservoir thicknesses. Incorporating fenestrations also may reduce corneal hypoxia-related stress.24 Finally, if scleral lenses are considered a final solution in an advanced corneal condition for which every other option has failed, clinicians must consider the risk-to-benefit ratio. The hypoxia-related stress generated by a thicker lens or by an increased fluid reservoir may be considered a minor consequence to restore sight, minimize pain, or rehabilitate the ocular surface.


When corneal edema reaches ~5%, a loss of tissue transparency is observable; at 10%, another feature, stromal folds, may be visible.25 Therefore, it is not surprising that signs of corneal edema secondary to modern scleral lens wear in healthy eyes (1% to 3%) are often not clinically visible under slit lamp examination. However, this does not mean that subclinical corneal hypoxia-related stress is not present.

Vascularization is a local limbal response to hypoxia or mechanical stress. In the case of scleral lenses, the fluid reservoir over the limbus rarely exceeds 100 microns, which makes it almost impossible to generate any significant local hypoxia-related stress. Consequently, vascularization may not be observed except in cases of compromised corneas (post-graft), continuous periods of lens wear, or limbal touch. The mechanical stress associated with the lens landing on the limbus can disrupt epithelial tight junctions, resulting in fluid accumulation between the cells (incorrectly named bullae).26 In turn, these structural changes can trigger an immune reaction resulting in the invasion of blood vessels into corneal tissue.

Considering these aspects, it is challenging to accurately quantify and monitor hypoxia-related stress (subclinical edema) whenever a patient is fitted in scleral lenses.27 Practitioners may use global non-contact pachymetry measures—but this requires lens removal28 —and optical coherence tomography (OCT) imaging to determine the corneal swelling in individual corneal layers.14 Confocal microscopy is another possibility,29 but it is primarily a research tool and not easily accessible to eyecare practitioners.


Debris in the fluid reservoir may be another potential indicator of hypoxia-related stress. This accumulation of whitish debris (fogging) may severely limit visual acuity and require wearers to remove the lens during the day for rinsing and replenishing the tear reservoir.3 Recently, pro-inflammatory white blood cells, which may predispose the ocular surface to inflammation,30 were identified within the reservoir of scleral lens wearers.31 Fogging was 2.24 times more likely for every additional 50 microns of tear reservoir thickness over 200 microns. While fogging may be a cause or a consequence of corneal stress, the accumulation of debris is multifactorial and is influenced by the peripheral lens fit and by tear exchange. Lowering the tear reservoir thickness centrally (< 200μm) and over the limbus (< 70μm) may contribute significantly to eliminating debris accumulation in the reservoir.


There is currently no prospective clinical study that has examined the longer-term effects of scleral lens wear. However, we can reflect on clinical outcomes of patients fitted with low-Dk soft lenses worn for extended periods throughout the 1980s. Certainly, the corneas of some patients were compromised due to chronic hypoxia-related stress,32 although the magnitude of corneal edema induced during this era was likely much greater than 1% to 3%.33 In some cases, when chronic hypoxia-related stress impacted endothelial function, corneal decompensation occurred as a cataract surgery complication.33 Does this mean that patients fitted with modern scleral lenses, exposed to low-level hypoxia-related stress, will be at greater risk for such corneal complications over time? Time will tell, but in the meantime, practitioners should strive to do no harm and to carefully weigh the risks, benefits, and practicalities of various contact lens modalities for each individual.


Regardless of a patient’s condition, the ocular surface, or the lens design or diameter, any scleral lens can and should be fitted to minimize hypoxia-related stress. This means limiting lens thickness, increasing material oxygen permeability, limiting the tear reservoir depth, and, for certain patients, limiting wearing time. One study suggested that the lens thickness—and not the tear reservoir depth—was the significant factor leading to hypoxia-related stress.11 This is contrary to current theoretical modeling derived from the understanding of the permeability of fluids and solutions.34 However, if true, it is imperative to collaborate with manufacturers to produce thinner lens designs.

A possible concern when fitting thinner lenses is flexure and resultant residual astigmatism. One published study35 and one author’s unpublished work (Dr. Michaud) examined scleral lens flexure as a function of center thickness. Lens thickness can be substantially reduced (to a center thickness of 150 to 200 microns) without significantly influencing the refractive outcome. Anterior lens flexure and residual astigmatism are greater when a thinner, rotationally symmetric lens is applied to a toric sclera. However, if the lens is well aligned in every quadrant (toric or custom haptic), minimal flexure is generated. The geometric stability of the lens may be altered if the lens is too thin; however, reducing the center lens thickness from 350 to 400 microns (common for many manufacturers) to 200 to 250 microns may be feasible for a range of myopia corrections. Unavoidable increases in lens thickness due to the lens power (convex) or diameter (larger lenses need to be slightly thicker) should be offset by using a higher-Dk material (200 is now available) and/or by reducing tear reservoir thickness to limit physiological impacts.


Considering all of the evidence from controlled clinical studies, practitioners should endeavor to minimize the risk of potential corneal hypoxia whenever possible by modifying the lens design and fitting, the lens material, and patient wearing time. Practitioners can achieve this with any scleral lens. For each patient, practitioners should consider the potential risks and benefits of scleral lens wear. What can you do to limit the risks and maximize the benefits? Fitting to improve oxygen delivery and to lower any chronic hypoxia-related stress is certainly one element to consider. We suggest that, especially for compromised corneas with a weakened endothelial pump mechanism, and when sclerals are likely to be prescribed for many years, adapting fitting strategies to alleviate hypoxia is mandatory. CLS


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