"I’m having a hard time getting my dry eye under control and my vision is becoming worse. What treatment options should I talk to my doctor about?"
Esen K. Akpek, MD
The pre-corneal tear film is the first structure having a direct and significant influence on the visual function. When dry eye is present, the tear film is degraded often due to insufficient tear secretion (quantity) and/or poor tear film stability (quality) leading to early decay of the tear film measured as tear break-up time. Poor tear quality can be due to meibomian gland dysfunction-related lipid deficiency or inflammation-related mucin deficiency. Poor tear quantity is due to inflammation-related changes in the tear secreting glands leading to reduced production. When dry eye becomes clinically significant, such as in patients with Sjögren’s, both the quality and quantity of the tear film are reduced. Management of clinically significant dry eye is complex and should incorporate various strategies: make more tears, conserve tears, and replace tears.
Make more tears
In patients with Sjögren’s related dry eye, the first line of treatment should be topical anti-inflammatory medications to improve the aqueous tear secretion. Currently, available topical anti-inflammatory medications include cyclosporine, lifitegrast and various steroids. Although effective, use of topical steroids should be restricted to intermittent, short term only, due to considerable side effects. Topical non-steroidal anti-inflammatory medications should be avoided due to significant corneal toxicity. Recently approved regenerative treatments, such as electroceuticals, should be employed early on in order to stimulate main and accessory lacrimal glands as well as Meibomian glands. Improving meibum secretion is essential in the care of significant combined mechanism dry eye. Warm compresses and lid scrubs should be incorporated into the patients’ everyday self-care. Office based therapies for meibomian gland dysfunction with or without anterior blepharitis (mechanical heat based or light-based therapies and microblepharoexfoliation) are available. These therapies are effective, albeit for a period of time, hence their required repeating and are costly. Oral and topical antibiotics and oral fatty acids might also be useful in improving significant combined mechanism dry eye.
Various types of tear duct plugs made of various materials are available to conserve tears in patients with significant aqueous deficient dry eye. However, those should never be the first line treatment for patients with chronic inflammatory dry eye, such as patients with Sjögren’s. In cases where duct plugs are uncomfortable due to lid issues or when patients lose duct plugs several times, permanent sealing using thermal cautery, or suturing can also be employed. Tarsorrhaphy to decrease the interpalpebral fissure opening and reduce evaporation of tear film should be saved for severe dry eye usually with corneal complications such as non-healing epithelial defects or ulcerations. Use of large diameter scleral contact lenses can be very helpful to improve the corneal surface and vision but only appropriate for patients with adequate dexterity. Also, they are costly.
In patients without an underlying systemic or local inflammatory condition, using over the counter tear substitutes would be appropriate as first line treatment in the absence of significant ocular surface and tear film parameters. However, in patients with Sjögren’s related dry eye, preservative free tears should never be a substitute for other/above treatments. Using these drops excessively/frequently can bother the homeostasis of the existing tear film and should not be recommended. Using human tissues such as amniotic membrane or fluids such as autologous serum tears, platelet rich plasma or amniotic fluid have been used with good results. Patients who cannot have successful blood draw, might be able to use allogeneic serum tears from known donors.
There are also several controversial strategies. Patients who have severe corneal punctate erosions, even in the absence of frank ulcerations, tend to have reduced corneal sensation. This could be attributed to inflammation leading to decrease in corneal subepithelial nerve plexus density as imaged with confocal biomicroscopy. Recently approved topical nerve growth factor treatment can effectively reverse the process and improve tear secretion as well as corneal epithelial regeneration. In patients with severe ocular surface inflammation due to Sjögren’s who have tried the above treatments, successful results of systemic anti-inflammatories including corticosteroids, non-steroidal immunomodulators or biologics have been reported in the published literature.
In summary, Sjögren’s related dry eye can be severe, even in the absence of severe patient reported symptoms due to reduction in corneal sensation. Addressing both the aqueous and meibum layers of the tear film, improving the regeneration of corneal nerves and ocular surface epithelium are essential components of the management.
This article was first printed in the Foundation's patient newsletter for members.