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April 05, 2024
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Case report: Cryopreserved amniotic membrane used for glaucoma medication-induced dry eye

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More than half of all patients treated with glaucoma medications have ocular surface disease, which predominantly manifests as dry eye disease.

Glaucoma treatment has been associated with higher levels of ocular surface alterations and inflammatory markers, which may explain the relationship between dry eye disease (DED) and glaucoma.

Fluorescein staining of the patient before AM placement
Figure 1. Fluorescein staining of the patient before AM placement.

Source: Zarmeena Vendal, MD

Case summary

An 82-year-old woman diagnosed with primary open-angle glaucoma for more than 10 years had received a topical regimen of timolol, brimonidine tartrate and latanoprost to manage her glaucoma. Previously, she had received artificial tears, over-the-counter lubricating gel and cyclosporine for her chronic glaucoma medication-induced dry eye symptoms, but she began complaining of tearing, fluctuating vision and foreign body sensation. This patient was at high risk for nonadherence to her glaucoma medications, reported a decrease in her quality of life, and was seeking other treatment for her dry eye symptoms.

Upon examination, the patient had trace injection redness of the conjunctiva and dense staining of her cornea (Figure 1). Her best corrected visual acuity in both eyes was 20/40. Based on the patient’s chronic dry eye symptoms and degradation of the corneal surface, a cryopreserved amniotic membrane (AM) was selected to help relieve the symptoms and ocular surface due to the regenerative and healing properties. A cryopreserved AM (Prokera, BioTissue) was placed on one eye at a time for a duration of 5 days. One week after treatment, the patient’s ocular surface was markedly improved, and she received follow-up 2 weeks later.

Two weeks after AM placement, her BCVA was still 20/40, with a reduction in the staining of her corneas. The patient self-reported improved comfort of her eyes and decreased foreign body sensation (Figure 2).

Fluorescein staining of the patient 2 weeks after AM placement
Figure 2. Fluorescein staining of the patient 2 weeks after AM placement.

At 4 months after AM placement, the patient reported sustained improvement of her dry eye symptoms and remained pain free. At 6 months, her cornea was stable and completely healed. The patient is now routinely monitored every 4 months for her glaucoma and dry eye symptoms.

Pathology of glaucoma-induced DED

Glaucoma is characterized by a progressive loss of retinal ganglion cells, resulting in changes at the optic nerve head and subsequent vision loss. Although the pathogenesis is not fully understood, loss of retinal ganglion cells is related to the level of IOP, which can cause mechanical stress and strain on the posterior segments of the eye. Reduction of IOP is the only proven method to treat the disease and is typically managed with ocular hypotensive drops; however, these medications are typically associated with ocular surface toxicity and the development of DED.

A key feature of DED is a persistent unstable and/or deficient tear film, resulting in visual impairment, and variable degrees of ocular surface epitheliopathy, inflammation and neurosensory abnormalities. Tear film abnormalities are also typical with chronic use of glaucoma drops and are associated with ocular surface alterations, meibomian gland loss, increased inflammatory cell infiltration and corneal fluorescein staining.

As the number of concomitant glaucoma medications increases, so does the prevalence and severity of dry eye symptoms in these patients. Patient-reported quality of life scores also decrease with increasing dry eye symptoms and number of glaucoma medications. Unmanaged DED can reduce patient adherence to glaucoma therapy, compromising the patient’s quality of life and resulting in treatment failure.

Treating glaucoma-induced DED with AMs

Severe and chronic glaucoma treatment-induced DED, much like the patient’s diagnosis in this case, may lead to severe corneal epithelial damage, thus necessitating adjunctive AM therapy, which is covered by most insurances. AMs can be used as an adjunct to heal and restore damaged ocular tissue relatively quickly. The collagen composition of AM closely resembles the conjunctiva and cornea, making it an ideal substrate for the growth of epithelial ocular cells.

The low immunogenicity and presence of various growth, anti-inflammatory and anti-angiogenic factors contribute to the ability of AM to promote epithelial growth and differentiation, all while reducing fibrosis during the healing process. AMs are preserved with two methods: dehydrated and cryopreserved. Although the preservation processes have similar clinical outcomes for patients with mild conditions, I prefer cryopreserved AM due to the live protein matrix and structural integrity of the basement membrane that is retained with the cryopreservation process.

Conclusion

A short course of 5-day treatment with AM per eye is beneficial for patients with glaucoma treatment-induced DED, and early initiation often leads to favorable clinical responses. Recognizing DED symptoms and initiating AM treatment early can optimize ocular surface health and patient outcomes. As suggested with this case, patients with iatrogenic DED can greatly benefit from AM treatment.