Crystalline Obstructive Sleep Apnea and the Eye

This article is from February 2008 and may contain outdated material.

Sleep is something we all need and, especially as physicians, often cherish. While eyelids that are tired and droopy may be one of the first signs to herald sleepiness, sleep disorders such as obstructive sleep apnea (OSA) actually have many ocular sequelae, some of which are vision-threatening. It is important for ophthalmologists to understand and identify sleep disorders—especially OSA—and their ocular associations, as these can occasionally be the source of unusual and often perplexing conditions.

About OSA

The increasing prevalence of obesity in our society has been associated with an upsurge in OSA, a disease that results in the cessation of breathing during sleep for 10 seconds or longer due to partial or complete obstruction of the upper airway. It is estimated that as many as 24 percent of Caucasian men and 9 percent of Caucasian women in the United States have OSA, though many of these cases remain undiagnosed.¹

Taking a good sleep history is the key to diagnosis and includes questions about day- and nighttime symptoms, specific obstructive breathing symptoms, and medical history of conditions associated with increased risk of OSA. Common daytime symptoms include sleepiness, difficulties with concentration and memory, and depression. Patients may also experience decreased productivity, anxiety, gastroesophageal reflux and sexual dysfunction. Nighttime symptoms include insomnia, frequent awakenings, and nocturia. Obstructive symptoms include loud snoring, choking and gasping, and witnessed apneas, which may be reported only by the patient’s bed partner. As patients age, the classic history of obesity, snoring and witnessed apneas is less common, and a careful history of sleep disturbances may be more revealing. Additional examination findings include increased neck circumference, tonsillar hypertrophy, enlarged soft palate, retrognathia and lower extremity edema.

Conditions associated with increased risk of OSA include positive family history of the disease, hypertension, diabetes, pulmonary hypertension, menopause and increased alcohol use. OSA patients also have an increased risk of automobile accidents as well as a higher risk of heart failure, stroke and death. Numerous ocular disorders have been found to be more prevalent in patients with OSA, including floppy eyelid syndrome, glaucoma, nonarteritic anterior ischemic optic neuropathy and papilledema with raised intracranial pressure.

Floppy Eyelid Syndrome

Floppy eyelid syndrome (FES) is probably the most common ocular disorder that has been associated with OSA. It is characterized by rubbery, redundant upper eyelid tissue and papillary conjunctivitis, and is seen most commonly in obese middle-aged men.²

The affected eyelid may correspond to the side on which the patient prefers to sleep. The etiology is uncertain, but current theories include an upregulation of elastin-degrading matrix metalloproteinases possibly caused by direct eyelid trauma, ischemia-reperfusion injury due to pressure placed on the eyelid, or low arterial oxygen tension during sleep.

When FES is severe, the eyelid may spontaneously evert during sleep and rub on the patient’s pillow, causing an acute exacerbation of mechanically induced conjunctivitis.

When a thumb is placed on the lateral upper eyelid and traction is applied, a striking laxity will be found and the eyelid will easily evert. These patients typically present with eye irritation, tearing and blurred vision, all of which are worse upon awakening. Examination findings may include beefy, red, palpebral conjunctiva with velvety papillary changes, diffuse punctate keratopathy, eyelid and eyelash ptosis, and loss of eyelash parallelism. As many as 10 percent of patients may have associated keratoconus.³

While the prevalence of OSA in patients with FES has been reported to be as high as 90 percent, only 2 to 5 percent of patients with OSA may have FES.⁴ Thus, it is impractical to screen all patients with OSA for FES. However, all patients with FES who do not have an established diagnosis of OSA should have a thorough sleep history taken and, when appropriate, should be referred for sleep evaluation including polysomnography.

Treatment of FES initially involves the use of lubricating eye drops and ointment, in addition to preventing mechanical injury during sleep by taping of the eyelid or use of an eye shield. Patients with FES and OSA who are already being treated with continuous positive airway pressure (CPAP) need to have their masks properly fitted to avoid additional eye injury due to misdirected air further drying out the eyes. Surgical treatment includes a full-thickness tarsal wedge resection, usually pentagonal in shape, or horizontal eyelid tightening with a traditional lateral tarsal strip procedure.

Glaucoma

The link between glaucoma and OSA is controversial. Most studies have shown a higher prevalence of both primary open-angle glaucoma and normal- tension glaucoma among patients with OSA, with one study showing a prevalence as high as 27 percent.⁵ Several small studies have identified OSA in patients with glaucomatous optic disc cupping and associated visual field defects who do not respond to medical or surgical IOP-lowering treatments, but whose visual fields stabilize when treated with CPAP. One Chinese study showed that patients with OSA were four times more likely to have glaucomatous optic disc changes and visual field defects than age-matched controls.⁶ The higher rate of normal-tension glaucoma among patients with OSA strongly indicates the two are correlated.

Several theories have been used to link OSA to glaucoma, one of which is that optic nerve head (ONH) damage is caused by apnea-induced ischemia. This would explain the lack of IOP elevation and family history of glaucoma in most persons affected with OSA. In addition, the vascular endothelium of the ONH vessels has been shown to function poorly in those with sleep- disordered breathing, which can lead to poor autoregulation of ONH blood flow and further ischemic damage. This is especially important at night when nocturnal fluctuations in systolic blood pressure are poorly compensated.

Current evidence suggests that at the very least a sleep history should be elicited from any patient diagnosed with normal-tension glaucoma who either has none of the classic risk factors for glaucoma or who has failed medical and surgical therapy. Also, it is important to confirm that persons with OSA and suspected or documented glaucoma are being treated adequately for OSA.

Other Optic Nerve Pathology

Nonarteritic anterior ischemic optic neuropathy. Multiple studies have shown that the incidence of OSA is higher in patients with NAION than in the general, age-matched population. In fact, NAION is more commonly associated with OSA than it is with diabetes or hypertension. It has been suggested that patients with NAION be questioned about their sleep habits. One research group that did this elicited a history of OSA 2.5 times more often in patients with NAION than in controls.⁷

Papilledema. Also associated with OSA, papilledema is thought to be caused by nocturnal increases in intracranial pressure. Potential mechanisms include raised venous pressure due to forced inspiration against a closed airway or hypercapnia-induced cerebral venous dilation.

When neuroimaging is normal, a careful sleep history in a patient with papilledema is critical in order to determine whether OSA is a causative factor. In such patients, treatment of the OSA has been shown to improve or resolve the papilledema.

Conclusion

Because OSA is associated with sight-threatening disorders in addition to systemic conditions with significant associated morbidity and mortality, we as ophthalmologists cannot afford to miss the diagnosis of a sleep disorder. Asking a few simple questions about your patient’s sleep habits may be the difference between making a sight-saving diagnosis or just looking like you’re asleep on the job.

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1 Young, T. et al. N Engl J Med 1993;328:1230–1235.

2 Culbertson, W. W. and H. B. Ostler. Am J Ophthalmol 1981;92:568–575.

3 Culbertson, W. W. and S. C. Tseng. Cornea 1994;13:33–42.

4 Karger, R. A. et al. Ophthalmology 2006;113:1669–1674.

5 Bendel, R. E. et al. Eye 2007;advance online publication 4 May 2007.

6 Tsang, C. S. L. et al. Eye 2006;20:38–42.

7 Li, J. et al. Br J Ophthalmol 2007;91:1524–1527.

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Dr. Harris is an ophthalmology resident, Dr. Givre is an assistant professor of ophthalmology and neurology, and Dr. Fowler is an assistant professor of ophthalmology. All are at the University of North Carolina at Chapel Hill.