Ophthalmologic Manifestations of Obstructive Sleep Apnea

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Disease Entity

Obstructive sleep apnea (OSA) is a common sleep disorder characterized by repetitive episodes of partial or complete upper airway obstruction associated with hypoxemia and re-oxygenation sequences.[1][2][3]

The widely accepted definition of OSA is an apnea-hypopnea index (AHI) more than 5, associated with symptoms such as excessive daytime sleepiness, fatigue, or impaired cognition.[3][4] The number of events per hour comprises the Apnea-Hypopnea Index (AHI).[1] Apnea is the complete cessation of airflow for at least 10 seconds, while hypopnea is a relative reduction in airflow accompanied by hypoxia or arousal from sleep.[1]


Epidemiology

The prevalence of OSA is approximately 3%-7% for men and 2%-5% for women.[1] Nevertheless, some American cohort studies, assessed the prevalence to be 17%-31% for men and 6.5%-9% for women.[4] Patients with OSA are more frequently male, obese and aged 65 years or more. Obesity is the most important risk factor: a 10% weight gain increases the risk of developing OSA by six-times.[3]

OSA prevalence increases 2-3 times in persons more than 65 years old. However, OSA is also described in children with adenotonsillar hypertrophy. African-American people are also more frequently affected.[3]


Pathophysiology

Anatomic and neuromuscular factors are involved in the development of obstruction of the upper airway in OSA. It is a combination of anatomically imposed mechanical loads on upper airways and the impaired activity of the pharyngeal dilator muscle during sleep, which normally contributes to the maintenance of pharyngeal patency.[3]

There are many alterations in the upper airway anatomy that reduce the size of the pharynx, such as the presence of tonsillar and tongue hypertrophy, retrognathia, and inferior displacement of the hyoid bone. Moreover, obesity can cause accumulation of fat in peripharyngeal tissues and increase pharyngeal collapsibility through reduction in lung volumes.[3]

It is hypothesized that the changes in oxygen saturation during sleep result in activation of the sympathetic nervous system which give rise to an increase in blood pressure, insulin resistance, changes in heart rate and arrhythmias, endothelial dysfunction, systemic inflammatory markers, release and enhanced platelet aggregation.[2] [5] It is known that these are mechanisms involved in the pathogenesis of cardiovascular disease (CVD), diabetes and other neurological disorders.[5] The main mechanisms leading to ocular complications are intermittent hypoxia, sympathetic overstimulation, oxidative stress, and damaging effects of endothelin-1 (ET-1).[5]


Clinical Presentation

The characteristic clinical presentation involves signs of upper airway obstruction during sleep, insomnia, and diurnal hypersomnolence. Symptoms normally begin insidiously and are typically present for years before patients seek medical attention. Nocturnal obstructive breathing symptoms include snoring, snorting, gasping, and choking, leading to intermittent awakenings and insomnia, with reduced total sleep time, fragmented sleep or early morning awakenings. The major diurnal complaints are chronic fatigue and daytime sleepiness. Severity of symptoms progress over the years and may rise with weight gain, aging or transition to menopause.[3]

Assessing for OSA is important, in part due to its strong association with hypertension, metabolic syndrome, diabetes, heart failure, coronary artery disease, arrhythmias, stroke, pulmonary hypertension, neurocognitive and mood disorders.[3]


Ophthalmologic Manifestations

Several ophthalmologic conditions are associated with OSA, including floppy eyelid syndrome (FES), glaucoma, nonarteritic anterior ischemic optic neuropathy (NAION), papilledema, keratoconus, and central serous chorioretinopathy (CSCR).[6]

Floppy Eyelid Syndrome (FES)

A condition where the upper eyelid becomes elastic and is easily folded upward.[6] The prevalence of OSA in patients with FES can be as high as 96%. However, the prevalence of FES in patients with OSA has been reported to be approximately 2%-33%.[6] It is often associated with papillary conjunctivitis, eyelid edema, and corneal epithelial erosions.[6] [7] In patients with obstructive sleep apnea, FES is thought to be caused by mechanical trauma to the eyelids during sleep. It is found commonly in obese patients due to weak tarsus.[5] Usually the affected eye corresponds to the side the patient sleeps on, and if both eyes are affected, it can suggest that the patient interchanges sides or that they sleep face down.[8]

Glaucoma

Optic neuropathy associated with injury to the optic nerve, thereby causing visual field defects. It can be correlated with increased intraocular pressure (IOP) or normal or reduced IOP (normal tension glaucoma). The prevalence of glaucoma in patients with OSA ranges from 2% to 27%.[6] The pathogenesis of glaucoma in patients with OSA is a combination of vascular and mechanical factors. Vascular factors include periods of hypoxia followed by oxidative stress during reperfusion. Mechanical factors comprise increased IOP at night due to changes in sleep architecture and increased sympathetic tone.[6] [7]

Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)

Acute optic neuropathy characterized by sudden and painless unilateral vision loss, edema of the optic disk, and a relative afferent pupillary defect. It can also occur in the fellow eye. [6] [7] Patients with OSA have 16% more probability to develop NAION compared to patients without OSA, and the prevalence of OSA in patients with NAION may be as high as 71%-89%.[6] It is suggested that patients with OSA are more susceptible to developing NAION due to a combination of hypoxia, oxidative stress, and increased intracranial pressure (ICP) during apnea episodes.[6]

Papilledema

Bilateral swelling of the optic disk. When the disc edema is caused by an increase in ICP and not by other mechanism, it is called pseudotumor cerebri, or idiopathic intracranial hypertension (IIH), and OSA should be considered in patients who do not have typical risk factors for IIH. Patients with IIH are often obese, as are patients with OSA. Patients with OSA have been shown to have increases in their ICP during sleep due to hypoxemia during apnea episodes.[6] Other theories include compression of the transverse venous sinuses causing elevated intracranial pressure.[9]

Keratoconus

Bilateral condition characterized by progressive thinning of the cornea and high irregular astigmatism. The central cornea projects outward, creating the appearance of a cone. Approximately 18% to 20% of patients with keratoconus have OSA [6] Male patients with keratoconus who have a high BMI or a family history of OSA are more likely to have OSA. The pathophysiology for developing keratoconus in patients with OSA is not well comprehended, but it is proposed that obesity may have a role in both conditions. One proposed theory regarding causation relates to mechanical injury to the cornea during sleep.[6]

Central Serous Chorioretinopathy (CSCR)

Condition in which serous detachment of the neurosensory retina develops at the macula. Approximately two-thirds of patients with CSCR have OSA. One theory for this increased prevalence is the presence of augmented oxidative stress, which can produce endothelial cell damage and vasoconstriction.[6] It is also stated that the relationship between CSCR and OSA can be a consequence from the mutual factor of obesity.[6]


Diagnosis

Medical history and physical examination are the cornerstones of diagnosis of OSA.

History Physical Examination
Daytime symptoms
  • Hypersomnolence
  • Morning headaches
  • Dry mouth
  • Irritability
  • Forgetfulness
  • Depression

Nocturnal symptoms

  • Snoring
  • Choking
  • Snorting
  • Gasping
  • Insomnia
  • Nocturia
  • Obesity
  • Large neck circumference
  • Retrognathia
  • Micrognathia
  • Macroglossia
  • Crowded airway appearance

[3]

Diagnostic criteria
A. Excessive daytime sleepiness that is not better explained by other factors.

B. Two or more of the following that are not better explained by other factors: Choking or gasping during sleep; Recurrent awakenings from sleep; Unrefreshing sleep; Daytime fatigue; Impaired concentration.

C. Overnight monitoring demonstrates ≥5 obstructed breathing events per hour during sleep.

Diagnosis of OSA is confirmed by the presence of criterion A or B, plus criterion C or by the presence of 15 or more obstructed breathing events per hour of sleep regardless of symptoms.

[3]

Classification of severity of OSA on the basis of apnea-hypopnea index (AHI).

Mild Moderate Severe
AHI 5-14 AHI 15-29 AHI ≥30

[3]

Questionnaires such as the STOP-Bang Questionnaire (SBQ), the Epworth Sleepiness Scale (ESS) and the Berlin Questionnaire are used for OSA screening, as well as ongoing monitoring of symptom progression / improvement.[4] The overnight diagnostic polysomnography (dPSG) is the gold standard for the diagnosis. More affordable portable devices exist to perform home polysomnography.[4]


Treatment

The two management options shown to improve outcomes in patients with OSA are weight loss and continuous positive airway pressure (CPAP).[4] CPAP constitutes a physical pressure support to prevent partial or complete collapse of the airway during sleep. It can be very effective in reducing symptoms and the potential complications of OSA.[3]

For patients with mild OSA or poor CPAP tolerance, oral appliances are available to splint the upper airway by advancing the lower mandible or retaining the tongue. Surgery is an effective therapeutic alternative in specialized circumstances including craniofacial abnormalities or discrete obstructing lesions.[4]

In patients who fail medical therapy, hypoglossal nerve stimulation (HSN) has shown promising results in reducing AHI and ESS scores. Studies have revealed that HSN improves the level of alertness and decreases the duration of time awake after sleep onset. Also, a lateral sleeping position is a potential conservative treatment option.[4]

References

  1. 1.0 1.1 1.2 1.3 Wong, B., & Fraser, C. (2019). Obstructive Sleep Apnea in Neuro-Ophthalmology. Journal of Neuro-Ophthalmology, 39, 370-379.
  2. 2.0 2.1 Huon, L.-K., Liu, S. Y.-C., Camacho, M., & Guilleminault, C. (2016). The association between ophthalmologic diseases and obstructive sleep apnea: a systematic review and meta-analysis. Sleep Breathing Physiology and Disorders , 1-10.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 Mannarino, M. R., Filippo, F. D., & Pirro, M. (2012). Obstructive sleep apnea syndrome. European Journal of Internal Medicine , 23, 586-593.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Fraser, C. L. (2019). Update on obstructive sleep apnea for neuro-ophthalmology. Curr Opin Neurol , 32, 124-130.
  5. 5.0 5.1 5.2 5.3 Morsy, N. E., Amani, B. E., Magda, A. A., Nabil, A. J., Pandi-Perumal, S. R., Bahammam, A. S., et al. (2019). Prevalence and Predictors of Ocular Complications in Obstructive Sleep Apnea Patients: A Cross-sectional Case-control Study. The Open Respiratory Medicine Journal , 13, 19-30.
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 Skorin, L., & Knutson, R. (2016). Ophthalmic Diseases in Patients With Obstructive Sleep Apnea. The Journal of the American Osteopathic Association , 116, 522-529.
  7. 7.0 7.1 7.2 West, S. D., & Turnbull, C. (2016). Eye disorders associated with obstructive sleep apnoea. Curr Opin Pulm Med , 22, 595-601.
  8. McNab, A. A. (2007). The eye and sleep apnea. Sleep Medicine Reviews , 11, 269-276.
  9. Thurtell, M. J., Trotti, L. M., Bixler, E. O., Rye, D. B., Bliwise, D. L., Newmann, N. J., et al. (2013). Obstructive sleep apnea in idiopathic intracranial hypertension: comparison with matched population data. J Neurol. , 260 (7), 1748-1751.