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Section 15. Dermatologic and Sensory Organ Disorders
Chapter 126. Aging and the Eye
Topics:    Introduction | Age-Related Changes in Ocular Structure |
Age-Related Changes in Ocular Function

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Age-Related Changes in Ocular Structure

Figure 126-1 depicts the anatomy of the eye, including structures that undergo age-related changes.

Sclera: The sclera forms the posterior 5/6 of the eyeball. In young and middle-aged adults, the sclera is white; in elderly people, it may have a yellowish tinge mimicking jaundice. The change results from dehydration and lipid deposits. Other age-related changes may include yellowing or browning due to exposure to ultraviolet light, wind, and dust; more random splotches of pigment, which often occur in people with a dark complexion; and a bluish cast due to thinning of the sclera that may occur with some diseases (eg, rheumatoid arthritis).

Conjunctiva: The conjunctiva is a thin mucous membrane that lines the eyelids and the anterior surface of the eyeball. Its goblet cells produce mucin, which lubricates the eyelids (enabling eyelids to move more smoothly) and provides a protective layer to slow evaporation of the tear film. With aging, the number of mucous cells decreases, contributing to dry eyes. Capillaries in the conjunctivae become more fragile with aging and burst more easily, resulting in pooling of blood in the space between the sclera and the overlying conjunctiva (subconjunctival hemorrhage). Subconjunctival hemorrhages, while alarming in appearance, are benign and resolve without treatment within 2 wk.

Limbus: The limbus is the junction between the sclera and the cornea. Although it is only 1.5 to 2 mm wide, the limbus contains the trabecular meshwork and the Schlemm's canal, which are important in maintaining correct intraocular pressure.

Aqueous humor: The aqueous humor is a fluid filtrate of blood plasma continuously produced by the ciliary body. It flows around the lens and is reabsorbed through the Schlemm's canal in the limbus back into the blood. The aqueous humor exerts outward pressure (intraocular pressure) that varies throughout the day, being highest in the morning and lowest in the evening (at the resting level). With aging, resting intraocular pressure can rise over time by as much as 25% without damaging vision. The mechanism for this normal increase is unknown, but it may be caused by an increase in the production rate of aqueous humor or a partial obstruction of the Schlemm's canal over time. Glaucoma results if intraocular pressure becomes higher than is healthy for the optic nerve. The composition of aqueous humor does not change with aging.

Vitreous humor: The vitreous humor is a clear, gelatinous substance consisting of collagen and sodium hyaluronate that fills the eyeball between the retina and the lens and helps maintain sufficient intraocular pressure to keep the eyeball from collapsing. It is firmly attached anteriorly at the peripheral retina and posteriorly at the optic nerve. The vitreous humor is normally clear, but with aging, discrete opacities (floaters) or structural changes such as cholesterol deposits (synchysis scintillans) may cause glare or a general haziness. With aging, vitreous fibrils become more demarcated, followed by the formation of liquid-filled pockets as the sodium hyaluronate separates from the collagen and liquefies. These pockets eventually enlarge and become confluent because the cortical vitreous also degenerates with aging and disintegrates. The liquefaction of the vitreous and the destruction of the cortex that holds the vitreous in place allow collected fluid to empty into the space between the retina and the vitreous, thereby causing vitreal detachments.

If the vitreous liquefies, normal eye movements can produce intermittent tension at the attachment points on the retina. This tugging can stimulate the peripheral retina mechanically, sometimes causing vertically oriented flashing lights, almost always in the far temporal visual field. These flashing lights may not be normal and may indicate that the retina is at risk of detaching.

Cornea: The cornea is transparent and forms the anterior 1/6 of the eyeball; it is the most important refractive portion of the eye. Arcus senilis (a deposit of calcium and cholesterol salts appearing as a gray-white ring at the edge of the cornea, 1 to 2 mm inside the limbus) is extremely common after age 60 and has no clinical significance.

Corneal sensitivity to touch decreases with aging, with the biggest changes occurring after age 40. The patient does not typically notice the change, and the change is sufficiently small that susceptibility to abrasions is not increased.

Iris: The iris comprises 2 sets of muscles that work together to regulate pupillary size and reaction to light. With aging, these muscles weaken, and the pupil becomes smaller (more miotic), reacts more sluggishly to light, and dilates more slowly in the dark. As a result, people > 60 may complain that objects are not as bright (smaller pupils admit less light), that they are dazzled initially when going outdoors (slower pupillary constriction), and that they experience difficulty when going from brighter to darker environments (slower pupillary dilation). If visual acuity is not decreased, the patient should be reassured that these changes are normal.

Both pupils should be the same size when they receive equal light. If the pupillary response is absent, the patient may be taking a drug (prescribed or over-the-counter) that causes pupillary constriction or dilation. Unequal pupil size is cause for concern, especially if the pupils were known to be of equal size, because unequal size indicates the possibility of a brain lesion in any number of places, such as the retina or the optic nerve (optic neuritis), the midbrain (pinealoma), the intercalated neuron (Argyll Robertson pupil), the optic nerve (an aneurysm), and the ciliary ganglion or short ciliary nerves (tonic pupil); referral to an ophthalmologist is indicated.

Lens: The lens is a transparent, metabolically active mass of proteins and water which, along with the cornea, refracts the light coming into the eye. Lens thickness and surface curvatures are changed by the actions of the ciliary muscle and zonule of Zinn (suspensory ligaments). The lens continuously grows during life, increasing in density and weight and decreasing in elasticity. Between the age of 40 and 50, the lens usually becomes so inelastic that close objects can no longer be brought into focus without the assistance of corrective lenses (presbyopia). The lens may also develop opacities that can cause glare and other visual changes.

Retina: The retina becomes less reflective of light with aging. The optic nerves tend to have less distinct margins and may appear slightly paler than they do in younger people because of a loss of capillaries due to small-vessel disease secondary to atherosclerosis. The macula, which in younger people usually has a bright central foveal light reflex, may have no foveal reflex in elderly people. Also, yellowish white spots (drusen) often appear in and around the macula, representing granular subretinal deposits of extracellular material. The retinal layers may become disrupted, resulting in pigmentation showing through and obscuring the view of underlying blood vessels. Unless these macular changes are accompanied by a distortion of edges of objects or a measurable decrease in visual acuity unexplained by other causes, they are not clinically important. Retinal signs of atherosclerosis include slight narrowing of the retinal arteries and an increased light reflex from thickened vessel walls. In addition, the retinal veins may show marked venous indentation (nicking) at the arteriovenous crossings with slight proximal distention.

Eyelids: The eyelids are controlled by the orbicularis oculi muscles, which squeeze the eyelids shut. With aging, the muscles in the lower eyelid may decrease in strength, resulting in ectropion (outward and downward turning of the eyelid away from the eyeball). Spasm of the muscles may cause entropion (inward turning of the eyelid margin), especially of the lower eyelid, resulting in trichiasis (the eyelashes contact the eyeball, rubbing it with each blink), and chronic irritation

Lacrimal gland and tear drainage: Tear production by the lacrimal gland may decrease with aging, resulting in fewer tears available to keep the surface of the eye, especially the cornea, well moistened. This change, combined with an age-related decline in conjunctival mucin production by the goblet cells, and decreased production of stabilizing surface oil by the Meibomian glands (located on the underside of the upper eyelid), may cause aqueous tear-deficient keratoconjunctivitis sicca. Abnormalities of the lacrimal system may result in either decreased or increased tear production. The excessive dryness caused by decreased tear production can often be treated by vigilant application of artificial tears. Referral to an ophthalmologist is indicated when the patient complains of excess tears and the punctum of the lower eyelid is not in contact with the eyeball. These tears spill over the lower eyelid and down the face, promoting excessive bacterial growth in the skin and eyelids, which can cause unsightly inflammation.

Orbit: With aging, there is a loss of the periorbital fat that surrounds and cushions the eyeball. This loss of fat often causes enophthalmos (sinking of the eyeball into the orbit), an asymptomatic condition that often poses a cosmetic problem and may be corrected with surgery.

This topic was last updated May 2005.

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