Sleep apnea and the eyes.
Glaucoma is a group of eye diseases in which the optic nerve is slowly destroyed resulting in vision loss. By the time vision problems manifest (e.g., seeing a halo around objects, blurred vision, eye pain, sense of pressure in the eye, peripheral vision loss, or night blindness), glaucomatous damage to the eye is usually very progressed.
In 1709, French physician Michel Brisseau demonstrated that glaucoma had a different pathological process from another eye disease - cataracts (a disease resulting in an opaque lens with which it was often confused). Clues into the process have slowly come to light since the 1850s when the ophthalmoscope first allowed physicians to directly see the pathological changes occurring within an glaucomatous eye.
The etiology of the pathological changes of the optic nerve in glaucoma is usually attributed to the presence of an excessive amount of aqueous fluid. In a normal eye, the ciliary body (a muscular structure located behind the iris) produces aqueous fluid and releases it into the posterior chamber of the eye. The aqueous fluid flows from the posterior chamber into the anterior chamber through the pupil. Once there, it provides nutrients, oxygen, and shape to the eye's anterior structures (e.g., iris, cornea). Aqueous humor ultimately drains out of the eye by two routes. In the first route (called the conventional or trabecular route), the fluid flows out of the anterior chamber through openings in a loose fibrous spongy tissue (the trabecular network) located at the junction between the iris and cornea. just above the trabecular network, the fluid passes through tiny pores into a vessel (the Schlemm canal). It exits the Schlemm canal through collector channels and enters into nearby sclera! veins which then take the fluid away from the eye. In the second route (the uveoscleral route), aqueous fluid flows through the muscle fibers of the ciliary body. The fluid enters nearby sclera! veins which take it away from the eye.
For poorly understood reasons, an eye affected by glaucoma has an impaired flow of the aqueous humor. Scientists are not sure whether aqueous humor does not drain out of the eye sufficiently or whether the ciliary bodies are producing an excessive amount of the fluid. Either scenario could result in the increased intraocular pressure seen in most forms of glaucoma.
The injury to the optic nerve that occurs in glaucoma is thought to occur in two steps. First, an initial injury occurs in the retinal ganglion cells (whose axons make up the optic nerve). For example, high intraocular pressure may compress vessels supplying the retinal ganglion cells to the point that oxygen exchange can not occur. The retinal ganglionic cells begin to die setting off the second stage. The second stage is a slow degenerative process. As nerve cells in the hypoxic tissue die they release noxious chemicals which systematically destroys surrounding healthy cells. Objectively on a opthalmologic examination, this destruction is seen as a shrinking of the optic disk. Subjectively, a person may note halos around objects, have changes in color perception, have blurred vision, and a loss of vision.
Normally, retinal blood vessels respond to changes in oxygen by expanding during hypoxia and constricting during hyperoxia. Sleep apnea results in frequent episodes of hypoxia (resulting from apnea or hypoventilation) followed by hyperventilations to quickly restore oxygen level. Such frequent oxygen changes may compound problems with blood flow that are already occurring in a glaucomatous eye.
Various researchers have noted a correlation between sleep apnea and glaucoma. A 2004 study by Marta Misiuk-Hojlo et al. found that 19% of their subjects had lesions on the optic tract (from glaucomatous neuropathy) as evidenced by visual field disturbances. This group of subjects had severe sleep-disordered breathing: the apnea-hypopnea index (AHI) was greater than 60%; the average oxygen desaturation of the subjects was about 86%; the minimal oxygen saturation (Sa02) was below 70%. Misiuk-Hojlo et al. concluded that lesions on the subjects' optic nerve is a consequence of severe and repeated episodes of hypoxemia during sleep. J. L. Batisse et al. noted that there was a greater incidence of visual field disturbances in their subjects who had a significant degree of sleep-disordered breathing. Daniel S. Mojon et al. found a high incidence of sleep apnea in subjects with nor-mal-tension glaucoma (i.e., glaucomatous changes in the eye but a normal intraocular pressure). Since glaucomatous changes occurred without high intraocular pressure, Mojon et al. suspect that another factor may play a role in causing the subjects' glaucoma. That factor may be sleep apnea.
Anterior ischemic optic neuropathy (AION) is sometimes described as a "stroke of the optic nerve." It comes in two forms.
The first form of AION - arteritic AION - results from of inflammation of cells (giant cells) of the carotid arterial system. When this system becomes inflamed, the optic nerve and retina - which are fed by branches from the carotid arteries - become prone to the consequences of the inflammation. One consequence is reduced blood flow. Transient blurring of vision occurs followed by permanent vision loss.
The second form of AION - non-arteritic AION (NAION)-results from a temporary drop in blood pressure. The drop in blood pressure is enough that the blood vessels supplying the optic nerve can not provide enough oxygen. Without sufficient oxygen, optic nerve tissue dies.
On arising, people with NAION note worse problems with vision (such as loss of peripheral vision, loss in distinguishing shades, and impaired depth perception). Scientists suspect this may be because blood pressure usually falls to its lowest during the night. The effects of sleep apnea on hemodynamics may provide the conditions for eye damage in NAION.
Papillema is a eye disorder that usually results from increased intracranial pressure. intracranial hypertension can be secondary to factors such as stroke, aneurysm, tumor or it can be idiopathic. Intracranial hypertension causes brain tissue to press against the optic nerve. The pressure prevents axoplasm in the optic nerve from flowing freely. The axoplasm builds up near the optic head (i.e., the portion of the optic nerve directly behind the eye). Objectively on ophthalmoscope examination, this process manifests as a swollen optic disc. Subjectively, symptoms of papilledema are a graying of vision especially on rising or sitting up; transient flickering; blurring; constriction of visual field; and decreased color perception.
Sleep apnea may worsen symptoms of papillederna due to a common risk (actor for sleep apnea: obesity. One thought is that increased abdominal tissue in an obese person results in increased intra-abdominal pressure. This, in turn, raises the pressure needed to fill the heart with blood. Increased cardiac filling pressure impedes the flow of venous blood as it returns to the heart from the brain. As a result, the venous blood builds up in the brain thereby increasing the intracranial pressure and resulting in papilledema.
Diabetic retinopathy occurs in people with long-standing diabetes. Capillaries in the retina form small sac-like dilatations (i.e., microaneurysms) which break and leak fluid. In response, new capillaries form; these new capillaries, however, break and bleed more easily. This bleeding can impair vision. Later, fibrosis may occur causing the retina to detach resulting in blindness.
Studies show that sleep apnea worsens diabetic retinopathy. It may be that increased hemodynamic pressures that occur as a person struggles to breathe during an apneic episode may worsen the hemorrhaging that occurs in diabetic retinopathy.
Scientists have noted that treating sleep apnea can reverse or improve symptoms of glaucoma, AION, papillederna, diabetic retinopathy and other eye diseases. Mojon et at. in a 1998 study treated apneic subjects with continuous positive airway pressure (CPAP). The subjects suffered from visual field defects despite having normal ophthalmologic examination. The visual defects remained did not worsen during an 18 month period in most subjects treated with CPAP and even improved in one subject. Mojon et al. concluded that CPAP treatment may stabilize or reverse visual field defects resulting from sleep apnea.
Andrew G. Lee et at. studied the effects of drug therapy only, drug therapy plus CPAP treatment, or CPAP treatment only on 6 subjects with papilledema (resulting from intracranial hypertension). All subjects had visual field defects before any treatment. After treatment (no matter the mode of treatment), five of the subjects had normal visual fields. Papillederna resolved in 3 subjects after treatment. These three, who were treated with drug therapy plus CPAP treatment, discontinued the drug therapy and stayed on CPAP alone. Lee et at. concluded that CPAP may improve symptoms of intracranial hypertension and its subsequent symptoms (e.g., papilledema).
Toshiaki Shiomi et al. report the case of a woman who had glaucoma and sleep apnea as a result ot Hallerrnann-Streiff syndrome. Hallerrnann-Streiff syndrome is a congenital disorder invoMng glaucoma in both eyes, microphthalmia (smaller-than-normal eyesl, dwarfism, lower-than-normal amount of body hair, a characteristic "beak-shaped" nose, micrognathia, dental abnormalities, and increased upper airway resistance. Shiomi et al. found that treating the woman with CPAP therapy prevented a worsening of her glaucoma symptoms during a time she had to forgo taking her normal drug regimen for glaucoma.
Physicians may need to check patients for sleep apnea who have been diagnosed with diseases that affect the vascular or neural tissues of the eye such as glaucoma, AION, papilledema, and retinopathy. Treating sleep apnea may save a patient's sight, reverse symptoms, or at least stall the worsening of symptoms.
by Regina Patrick, RPSGT
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|Title Annotation:||SLEEP MEDICINE|
|Publication:||FOCUS: Journal for Respiratory Care & Sleep Medicine|
|Date:||Jan 1, 2012|
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