Ocular Complications of Obstructive Sleep Apnea

Abstract

Obstructive sleep apnea (OSA), the most common form of sleep-disordered breathing, is characterized by repetitive episodes of paused breathing during sleep, which in turn induces transient nocturnal hypoxia and hypercapnia. The high prevalence of OSA and its associated health consequences place a heavy burden on the healthcare system. In particular, the consequent episodic oxygenic desaturation/reoxygenation series and arousals from sleep in patients with OSA have the potential to trigger oxidative stress, elevated systemic inflammatory responses, and autonomic dysfunction with sympathetic activation. Given these adverse side-effects, OSA is highly correlated to many eye diseases that are common in everyday ophthalmic practices. Some of these ocular consequences are reversible, but they may permanently threaten a patient's vision if not treated appropriately. Here, this article seeks to review the ocular consequences and potential pathophysiologic associations in patients with OSA. Understanding these OSA-related eye diseases may help clinicians provide comprehensive care to their patients.

Keywords: complications; eye; inflammation; nocturnal hypoxia; obstructive sleep apnea; oxidative stress; sleep-disordered breathing; sympathetic activation.

Figure 1

Schematic interactions of OSA and eye diseases in terms of common pathophysiological mechanisms. OSA has been directly/indirectly linked to many ocular diseases through three major mechanisms: oxidative stress, elevated systemic inflammation, and sympathetic activation. In glaucoma, hypoxia/hypercarbia directly damages high oxygen-depleted neuronal cells and triggers systemic inflammation and oxidative stress, leading to mitochondrial dysfunction and provoking ganglion cell apoptosis. Glaucoma is also directly aggravated by the mechanical damage caused by increased nocturnal intraocular pressure. In non-arteritic anterior ischemic optic neuropathy (NAION), nocturnal hypoxemia and impaired vascular autoregulation of posterior ciliary arteries may directly predispose NAION. Thyroid eye disease (TED), floppy eyelid syndrome (FES), central serous chorioretinopathy (CSC), dry eye syndrome (DES), and keratoconus (KC) may share some common excessive circulating cytokines and tissue inflammatory mediators with OSA. Hypercoagulopathy in OSA may contribute to retinal vascular occlusion (RVO) and diabetic retinopathy (DR)/diabetic macular edema (DME). OSA-induced vascular endothelial dysfunction and narrowing of blood vessels may lead to ischemia and damage to the delicate vessels in the optic nerve head and retina. Blood–retinal barrier (BRB) breakdown predisposes CSC and DR/DME. An increase in systemic oxidative stress may also induce the development of CSC. green = optic nerve; brown = posterior segment; purple = orbit and eye lid; blue = anterior segment.