The anatomical properties of the eyelids can cause difficulties when fitting GP lenses. Ptosis, eyelid tension, lower lid height, and palpebral aperture size can mechanically influence GP lens centration and fit, and the meibomian glands, eyelid epithelium, and other eyelid substructures are critical to proper tear composition and distribution. Ongoing research suggests that the reverse is also true: GP lenses cause negative changes to the eyelids with long-term use.

GP Lens Effects on the Lids

Deleterious effects from both soft and GP contact lens wear on meibomian gland number, structure, and function have been frequently described. It is not clear whether the damage comes from chronic lens-induced inflammation, particulate debris from lens application/removal and wear collecting in gland orifices, lens-worsened allergic reactions in ocular surface tissues, or a combination of these or other unknown factors (Mizoguchi et al, 2017). Regardless of etiology, meibomian gland damage appears to manifest through gland dropout, morphological changes, orifice plugging, and altered meibum secretions at a significantly higher rate than in non-contact lens wearers (Arita et al, 2017; Tang et al, 2016; Alghamdi et al, 2016).

Lid wiper epitheliopathy may have increased frequency in both soft and GP lens wearers (Shiraishi et al, 2014). Staining of the eyelid epithelium on both upper and lower lids along the posterior edge to the line of Marx and involving the conjunctival epithelium may indicate increased friction and/or inflammation during blinking, particularly over a lens.

A significantly increased risk of blepharoptosis has been noted in corneal GP lens wearers (Hwang and Kim, 2015), with some research indicating an up to 20-times higher risk in certain populations (Kitazawa, 2013). This should be taken seriously, as the only available corrective intervention is surgical. If the current increasing trend of orthokeratology for myopia control in young patients continues, we may expect to see younger patients presenting with ptosis-related vision and cosmetic complaints. GP lens-induced ptosis results from disinsertion or dehiscence of the levator aponeurosis similar to what occurs in senile ptosis, though the exact etiology is unknown. Lens removal techniques that involve eyelid pulling or stretching may be at least partially to blame (Thean and McNab, 2004). Other factors, such as lid attachment fitting with persistent lens weight and pull and/or fibrosis of Mueller’s muscle, might also contribute (Watanabe et al, 2006).

It is unclear whether scleral lenses or lenses that are removed primarily with the aid of suction-cup-type devices have any degree of risk of blepharoptosis. Any patient who will wear GP lenses for an extended amount of time should be warned of this potential complication and taught lens removal techniques that will minimize the potential for excessive ptosis development.

A Teaspoon of Prevention

Detrimental effects of GP lens wear on various eyelid structures and their function are still being discovered and are not fully understood, particularly when it comes to younger patients and new GP lens modalities such as scleral lenses. Fortunately, some relatively simple steps can be taken to reduce these risks, such as teaching lens removal techniques that don’t require lid stretching, minimizing chronic lens-induced inflammation, and regularly monitoring meibomian gland health. CLS

For references, please visit www.clspectrum.com/references and click on document #274.