Ocular surface disease exacerbated glaucoma


The rationale for optimizing the ocular surface in glaucoma patients

Case series


OSD caused by the long-term use of topical anti-glaucoma medication, can lead to conjunctival inflammation, foreshortening and shrinkage12 and severe symptomatic cicatrisation, which is indistinguishable from ocular cicatricial pemphigoid (OCP). The terms drug-induced cicatricial conjunctivitis (DICC) and pseudopemphigoid have been used.13

As discussed glaucoma therapy causes OSD, however, it is also apparent that severe OSD in turn exacerbates glaucoma. The prevalence of glaucoma in patients with severe OSD has been found to be 65.7%.14 Proposed mechanisms for raised IOP in patients with OSD are increased conjunctival inflammation in patients using anti-glaucoma medications, vascular aetiologies and inflammation of the trabecular meshwork, and in addition inflammation and scarring of the episclera and sclera thereby impairing the outflow facility of the eye.15 In support of this inflammatory theory, a higher rate of inflammatory cell infiltrates and fibroblasts have been found in conjunctival and trabeculectomy tissue samples from patients who are chronically exposed to preserved glaucoma medications.16

The aim of our treatment approach was to break the destructive cycle of events (OSD may potentiate glaucoma and vice versa) and achieve improved IOP control and a healthy ocular surface. In all four patients an improvement in the OSD resulted in an improvement in the IOP control and stabilization of the visual field. This obviated the need for surgical intervention, during the study period. We feel our approach was successful possibly due to decreased inflammation of the trabecular meshwork, conjunctiva, episclera and sclera leading to improved outflow facility of the eye.

If glaucoma filtration surgery is subsequently required in our patients, the improvement in the ocular surface may contribute to the increased likelihood of a successful surgical outcome.

It may be argued that the reduction in IOP may have been due to improved compliance with treatment for two reasons; firstly as patient care was transferred to a specialist consultant-led glaucoma service and secondly due to a reduction in ocular discomfort following treatment of the OSD. We feel that these scenarios are unlikely because all four patients reported good compliance with treatment prior to being referred to the service. Furthermore, we recognize the limitations of our small retrospective clinic-based observation and the need for large robust randomized studies to test our hypothesis.

Nevertheless, we feel that this is an important finding in a group of patients in whom management can be challenging; glaucoma in patients with severe OSD is often refractive to medical therapy14 and the surgical success of glaucoma filtering surgery is compromised in this group.17 Our study raises a new argument for maintaining increased awareness of the signs and symptoms of OSD in patients with glaucoma and emphasizes the importance of timely diagnosis and treatment of a phenomenon we describe as 'OSD exacerbated glaucoma'.

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Josefina Botta, MD, MSc, at ASCRS 2024
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