SLEEP MEDICINE
SLEEP APNEA AND THE EYES by Regina Patrick, RPSGT U
ntreated sleep apnea can contribute to problems with the car- diovascular system (e.g., hypertension), the heart (e.g., arrhyth-
mia), the kidneys (e.g., nephrotic syndrome), the liver (e.g., hypoxic hepatitis), and the central nervous system (e.g., stroke). In recent years, scientists have begun to realize that sleep apnea may con- tribute to problems in another organ – the eyes. Sleep apnea can increase the risk of developing glaucoma and can worsen the symptoms of anterior ischemic optic neuropathy (AION), pa- pilledema, and diabetic retinopathy. Glaucoma is a group of eye diseases in which the optic nerve
is slowly destroyed resulting in vision loss. By the time vision prob- lems 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 al- lowed physicians to directly see the pathological changes occur- ring 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 mus- cular 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 be- tween 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 scleral 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 scleral 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 intraoc- ular 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 supply- ing 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 chem- icals which systematically destroys surrounding healthy cells. Ob- jectively 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 com- pound 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 dis- turbances. 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 (SaO2) 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 in- cidence 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 oc- curred 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.
Focus Journal Winter 2012 7 continued on page 8
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44