Commentary: Obstructive sleep apnoea as a risk factor for glaucoma.

Sleep apnea is a type of sleep-disordered breathing that causes intermittent pauses in breathing during sleep, leading to transient nocturnal hypoxia and hypercapnia. Polysomnography is needed to confirm the diagnosis. Obstructive sleep apnea (OSA), the most common type, is due to complete or partial upper airway obstruction during sleep. Recurrent hypoxia due to desaturation and consequent arousal has several systemic effects affecting blood pressure, insulin resistance, autonomic dysfunction, and systemic inflammation.[1] Its severity is determined by the apnea–hypopnea index (AHI) (total number of apnea and hypopnea events divided by total sleep time), based on which it is classified as mild, moderate, and severe OSA.[2] It is associated with increasing age and obesity, making it epidemiologically relevant due to an aging populace and rampant lifestyle disorders in most countries today.[3] The ocular diseases most frequently associated with OSA are floppy eyelid syndrome, nonarteritic anterior ischemic optic neuropathy, glaucoma, central serous retinopathy, retinal vascular disorders, and dry eye disease.

The relationship between OSA and glaucoma has been the subject of many studies. It is of specific interest as another modifiable risk factor in glaucoma, besides IOP. It assumes importance in normal pressure glaucoma (NPG) and progressive glaucoma, despite adequate IOP control. A meta-analysis of cross-sectional and case-control studies showed an increased prevalence of glaucoma among OSA patients (pooled odds ratio (OR): 1.242, P < 0.001) and OSA diagnosis in glaucoma patients (pooled OR: 1.746, P = 0.002).[4] More importantly, a thinner retinal nerve fiber layer (RNFL), lower ganglion cell complex thickness (GCC) on optical coherence tomography, and decreased vessel density of superficial and deep-layer peripapillary and macular area on optical coherence tomography angiography are reported in patients with greater OSA severity (higher AHI).[56] The current study also provides evidence of thinner RNFL and GCC with OSA compared to normal controls in Indians.[7]

However, the exact pathophysiology of RNFL and GCC loss is unclear. There are multiple theories: (i) increased IOP due to supine posture, increased episcleral venous pressure, and autonomic dysfunction; (ii) optic nerve ischemia due to recurrent hypoxia; and (iii) vascular dysregulation at the optic nerve.[8] All of them remain to be proven. Other facts to be considered are that OSA patients are likely to have other comorbidities, such as ischemic heart disease, hypertension, and diabetes mellitus. Vascular diseases, in particular, are likely to be independent risk factors for glaucoma. There is some evidence that vascular factors may be responsible for OSA-related damage in NPG. Chuang et al.[6] reported decreased vessel density of the superficial and deep-layer peripapillary and macular area in OSA patients with NPG and perimetric damage. Evaluation of the role of vascular dysregulation and peripheral hypoxia in OSA-related glaucoma would require prospective cohort studies in OSA patients.

Though a clear relationship exists between OSA and NPG, high-pressure primary open-angle glaucoma (POAG) is also reported.[8] From a clinical standpoint, evaluating additional risk factors for glaucoma becomes essential in patients with rapidly progressive glaucoma (despite adequate control) and NPG. Thus, there may be a case for OSA evaluation by polysomnography, where indicated, in these patients. Obstructive sleep apnea treatment is lifestyle modification and continuous positive airway pressure (CPAP) therapy, which may mitigate early glaucoma. There may be concerns about IOP variations with CPAP. However, Lin et al.[9] demonstrated some reversal of structural and functional changes after short-term (3 months) CPAP therapy. Thus, early and appropriate intervention in OSA-related glaucoma may be beneficial.

Normal pressure glaucoma has a greater reported proportion among Asian (46.9%–92.3% of POAG) as compared to Western (30.0%–57.1% of POAG) countries, with similar data from South India (82%).[10] Thus, from an epidemiological standpoint, it would be important to study risk factors related to NPG in different populations. The estimated prevalence of OSA in India varies from 4.4% to 13.7% and is likely to rise with an aging population and increasing lifestyle diseases.[11] The current study is the first one from India that provides data regarding RNFL and ganglion cell complex changes in OSA.[7] Similar and extensive studies related to OSA and other potentially modifiable risk factors of glaucoma are the need of the hour.