Ocular Manifestations of Obstructive Sleep Apnea

Review Article

Austin J Sleep Disord. 2015;2(2): 1011.

Ocular Manifestations of Obstructive Sleep Apnea

Hatice Arda*, Duygu Gülmez Sevim, Ertugrul Mirza and Sarper Karakucuk

Department of Ophthalmology, Erciyes University Faculty of Medicine, Turkey

*Corresponding author: Hatice Arda, Department of Ophthalmology, Erciyes University Faculty of Medicine, Kayseri, 38039, Turkey

Received: March 11, 2015; Accepted: April 22, 2015; Published: April 24, 2015

Abstract

Obstructive sleep apnea (OSA) is a serious disorder characterized with repeated episodes of upper airway obstruction during sleep, resulting in nocturnal hypoxemia and hypercapnia which leads to many systemic and also ocular complications.

Various eye disorders reported to be associated with OSA. Floppy eyelid syndrome (FES), cornea disorders, glaucoma, non-arteritic anterior ischemic optic neuropathy, papilledema, central serous chorioretinopathy, and retinal vein occlusion are some of these disorders.

Keywords: Obstructive sleep apnea; Floppy eyelid syndrome; Optic neuropathy; Normal tension glaucoma

Abbreviations

OSA: Obstructive Sleep Apnea; PSG: Polysomnography; CPAP: Continuous Positive Airway Pressure; BiPAP: Bilevel Positive Airway Pressure; FES: Floppy Eyelid Syndrome; AHI: Apnea- Hypopnea Index; POAG: Primary Open Angle Glaucoma; NTG: Normal Tension Glaucoma; RNFL: Retinal Nerve Fiber Layer; IOP: Intraocular Pressure; NAION: Non-Arteritic Anterior Ischemic Optic Neuropathy; IIH: Idiopathic Intracranial Hypertension; CSCR: Central Serous Chorioretinopathy; RVO: Retinal Vein Occlusion

Introduction

Obstructive sleep apnea (OSA) is a serious disorder that leads to many systemic and ocular complications. It is characterized with repeated episodes of upper airway obstruction during sleep, resulting in nocturnal hypoxemia with the symptoms of excessive daytime sleepiness, disruptive snoring, and apnea episodes [1]. The prevalence of OSA is estimated to be approximately 9% in women and 24% in men [2]. Cardiovascular and neurological morbidity is a serious outcome of OSA with the fact that it is seen in approximately 60% to 70% of patients with stroke or ischemic heart disease [3]. The gold standard procedure in the diagnosis is the overnight polysomnography (PSG) [1]. The main medical treatment options for the condition are continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP), if CPAP is not tolerated by the patient [4]. Modafinil is a novel wake-promoting agent, reported to be an effective adjunct therapy for residual excessive sleepiness in patients treated with CPAP [5]. Surgical management options are limited to those in whom the medical treatment is not well tolerated or failed to be successful.

Its ocular associations have been an issue of great interest due to the irreversible complications it may cause and may have been preventable, if the condition of OSA is diagnosed and treated properly beforehand or even after the diagnosis of the ocular findings. Various eye disorders have been reported to be associated with OSA including; floppy eyelid syndrome (FES), cornea disorders, glaucoma, nonarteritic anterior ischemic optic neuropathy (NAION), papilledema, central serous chorioretinopathy (CSCR), and retinal vein occlusion (RVO). This review aims to take the attention of the ophthalmologists on the possibility of ocular disorders that can be accompanied by sleeping disorders.

Floppy eyelid syndrome

Mostly seen in overweight, middle aged males with the complaint of foreign body sensation, burning, tearing, and redness; FES is characterized with the clinical findings of flaccid and easily everted upper lids, occurring spontaneously or with minimal traction, and chronic papillary conjunctivitis of the upper palpebral conjunctiva. Tarsal plaque biopsies of the patients with FES revealed the histopathological features as an increase in the elastolytic metalloproteinase enzymes and a subsequent decrease in the elastin fibers of the tissue [6,7]. In the literature the prevalence of FES in the OSA population has been reported to vary from 2% to 32% [8,9]. OSA is known to be seen mostly in overweight patients, so there is not a clear distinction regarding the etiology concerning whether FES and OSA is related directly or FES is mainly related to obesity. The prevalence of obesity in OSA has ranged from 60% to 70% [10,11], while the prevalence of obesity in FES patients has ranged from 43% to 92% [12,13]. In their review of patients with lax eyelid syndrome, Fowler and Dutton [14] stated that there was not a significant difference regarding the prevalence of OSA between patients who had obesity and FES and who had obesity but did not have FES. They also found that patients with OSA tended to have the prevalence of obesity significantly higher than those without OSA (76% vs. 20%). So they concluded that increased OSA prevalence among patients with FES was possibly associated with the concomitant obesity. On the contrary of the findings of this study, Ezra et al. [10] found a strong relationship between OSA and FES independent of weight. They explained that the possible mechanism might have been the changes in central nervous system arousability in OSA. Another possible explanation for the underlying mechanism of the association between OSA and FES is believed to be the increased venous pressure caused by right heart failure and apnea in patients with OSA [15].

Regarding the ocular surface findings along with FES, Acar et al. revealed low levels of Schirmer I values and tear break up times, and an increase in corneal staining and ocular surface disease index scores in patients with OSA, with the changes being correspondingly related to the severity of the disease based on apnea-hypopnea index (AHI) [16]. The authors suggested that the floppiness of the eyelid increases the inflammation in the ocular surface, causing a reduction in the amount and the quality of the tear and the symptoms of FES such as burning, itching and redness. Although there have been reports indicating a negative effect of CPAP treatment on ocular surface parameters because of the irritative properties of the treatment, in the second stage of their previous study, Acar et al. [17] reported that all of the latter impaired findings, including the stage of FES showed a significant improvement in patients with moderate and severe OSA, after 18 months of CPAP treatment. They concluded that the treatment should be implemented in an appropriate manner for at least one year in order to encounter the ocular surface irritation that is seen in the early stages of the therapy.

In their recent study to determine whether the presence of FES is associated with a higher prevalence of glaucoma in OSA patients, Muniesa et al. [18] found a significantly higher prevalence of glaucoma among the patients with FES (23.07%) compared to patients without FES (5.3%), and concluded that FES could be used as an indicator of glaucoma in patients with OSA.

Glaucoma

Several reports in the literature indicated possible associations between OSA and primary open angle glaucoma (POAG), normal tension glaucoma (NTG), visual field defects and reduced retinal nerve fiber layer thickness (RNFL). However, there have been contradictory reports regarding the relationship between OSA and glaucoma, with one study showing no difference [19], while another indicating the prevalence of glaucoma in OSA being approximately 4 times higher than the expected population rate [20].

The pathogenesis of ocular complications in OSA is most likely to have multifactorial origin. Vascular and mechanical factors have been thought to be involved in the pathological mechanism of the optic nerve involvement. Vascular factors are mainly the outcomes of repetitive or prolonged episodes of hypoxia; that include direct damage to optic nerve, oxidative stress and inflammation, increased vascular resistance, autonomic dysfunction, increased intracranial pressure and decreased cerebral perfusion (Figure 1) [21]. Repetitive prolonged upper airway obstruction and following arousal lead to an increase in the sympathetic tone, thus causing an activation in the rennin-angiotensin system. These factors and the accompanying effect of hypoxia trigger an increase in blood pressure and vascular resistance, causing damaging in the vascular endothelium. All of these consequences lead to the impairment of the autonomic function, an imbalance of vasodilatation and vasoconstriction. Furthermore the effect of the arousal periods and reperfusion lead to inflammation and oxidative stress, shown by the increased levels of reactive oxygen species and inflammatory markers [21]. In the etiologic scope, mechanical factors include supine position and obesity related increased intraocular pressure (IOP), and intracranial pressure at night, and the depletion of fiber in the trabeculum and lamina cribrosa [21]. To reveal the clinical impact of the pathogenesis of vascular pathology, Karakucuk et al. [22] noted that among the OSA patients with glaucoma, all of the patients had severe OSA and they revealed a strong correlation between AHI and IOP, and between mean defect in the visual field testing and resistivity index of the ophthalmic artery and central retinal artery determined with orbital Doppler ultrasonography.

Citation: Arda H, Sevim DG, Mirza E and Karakucuk S. Ocular Manifestations of Obstructive Sleep Apnea. Austin J Sleep Disord. 2015;2(2): 1011. ISSN:2471-0415