P56 Is obstructive sleep apnoea a risk factor for reduction of retinal nerve fibre layer thickness in primary open-angle glaucoma?

Abstract

Introduction It has been hypothesised that Obstructive Sleep Apnoea (OSA) may contribute to glaucomatous progression through hypoxic stress and vascular dysfunction. The purpose of this study was to determine whether OSA is a risk factor for increased progression of retinal nerve fibre layer (RNFL) thinning in primary open-angle glaucoma (POAG). Methods Patients with POAG who took part in the POSAG study (Prevalence of Obstructive Sleep Apnoea in Glaucoma, NCT02713152) and underwent a comprehensive ocular examination and a nocturnal multi-channel cardiorespiratory monitoring were screened for eligibility. Longitudinal data on circumpapillary RNFL thickness measured using Ocular Coherence Tomography (OCT) were collected retrospectively. A minimum of 3 years of follow up period was required. Patients with central sleep apnoea, inadequate quality OCT scans, ocular co-morbidities and those who received treatment for OSA were excluded. For each patient, both eyes were included in the analysis. Results 167 eyes of 88 patients met the eligibility criteria and were enrolled. 54.5% of included patients were diagnosed with OSA which was moderate to severe in 21.6% of all patients. Average global RNFL thickness loss in patients with OSA was −1.1±1.6 µm/year compared to −0.6±1 µm/year in those without OSA (p=0.013). In a multivariable model adjusted for age, cardiovascular co-morbidities, intraocular pressure and prior filtration surgery, OSA was independently associated with global RNFL thinning (p=0.002). The largest differences in RNFL thinning between the groups were in superior and inferior sectors which are typically first affected in POAG. Discussion To our knowledge this is the first study which examined POAG progression measured by longitudinal OCT changes and in relation to untreated OSA. We have found that POAG patients with OSA were losing global RNFL thickness on average almost twice faster than those without OSA and that this was independent of other factors. This study indicates that OSA may be a risk factor for progressive structural damage of the optic nerve in patients with POAG. However, these findings should be confirmed in a larger prospective study and it is still unclear whether the impact of OSA is large enough to produce functional visual field impairment.