aqueous the beam will be invisible, the out-of-focus cornea and lens will be visible in the reflected light, but the aqueous will be dark or “optically empty.” If there are particles in the pathway of the beam, light will be reflected and scattered producing the Tyndall phenomenon, making the beam visible within the aqueous.

Cells and flare in the anterior chamber can be indicative of uveal inflammation or infection. A disruption of the zonula occludens between the nonpigmented ciliary cells causes a breakdown of the blood-aqueous barrier and can occur in inflammatory conditions, allowing immune factors and leucocytes into the eye to fight invading microbes, causing cells and flare.35 This accumulation of material usually

appears whitish and if there is significant amount it may settle in the inferior anterior chamber, forming an hypopyon.

Trauma involving a blow to the head or an injury such as whiplash can cause a tear or break at the iris root and result in damaging the iris blood vessel branches entering from the major circle of the iris. Such a hemorrhage will cause blood to enter the anterior chamber and due to gravity will settle inferiorly. This accumulation of blood forms a hyphema.

FUNCTIONS OF CHOROID

The vascular choroid provides nutrients to the outer retina and is an egress for catabolites from the retina, passing through Bruch’s membrane into the choriocapillaris. The darkly pigmented choroid absorbs excess light as does the RPE layer. The suprachoroidal space provides a pathway for the posterior vessels and nerves that supply the anterior segment.

With aging, excessive basement membrane (basal lamina) material is deposited in the collagenous zones of Bruch’s membrane.44-46 These deposits in the inner collagenous zone, called drusen, can be seen as small, pinhead-sized, yellow-white spots in the fundus (Figure 3-22). The drusen, which contain cellular fragments and an accumulation of basal laminar material, are located outer to the RPE basement membrane and displace the retina inward.47

Clinical Comment: Age-Related

Macular­ Degeneration

Degenerative processes involving the choroid-retina interface in the macular area often are manifested as age-related macular degeneration (AMD). AMD is the most common cause of blindness in Western countries.48 This disease is multifaceted in origin and can involve the presence of multiple or confluent drusen, a thick layer of basal laminar deposit, detachment or atrophy of the RPE, subsequent formation of disciform scars, (Figure 3-23) loss of photoreceptors, and neovascularization.47,49

Metabolites from the choriocapillaris and waste products from the retina must pass through Bruch’s membrane. With age, phospholipids accumulate in this membrane, probably

because of defective mechanisms in the dephosphorylation process.45,50-53 Free radicals resulting from oxidative stress have been implicated in these cellular metabolic changes.54 The accumulation of lipids in Bruch’s membrane with increasing age appears to be greater in the central fundus than in the periphery.55 Bruch’s membrane becomes hydrophobic and presents a barrier to water movement, thereby inhibiting the passage of metabolites.56 If water accumulates between the RPE and Bruch’s membrane, displacement and detachment may occur.52 This process is represented diagrammatically in Figure 3-24.

Loss of nutrients to the highly metabolic retina can cause (1) atrophy of the RPE, followed by loss of photoreceptors,53,57 or (2) development of a neovascular membrane in an attempt to compensate for the loss

of nutrients.54,56 The new vessels branch from the choriocapillaris and can remain beneath the RPE or can penetrate Bruch’s membrane and enter the retina.54 However, these vessels are fragile, leak, and tend to hemorrhage into retinal tissue.52,58 Visual loss in AMD results from detachment of the RPE resulting from water accumulation, atrophy of the RPE and photoreceptors, or the presence of a subretinal neovascular membrane.45,50

Risk factors associated with AMD include genetics; age; lighter pigmentation of skin, hair, or iris; skin sensitivity to sun; smoking; sun exposure; and cataract surgery.54,56,59-63 Although these risk factors have been elucidated, their role in AMD is still not seen as causative. The complex interplay among these factors, however, implicates many if not all of them in AMD.

No definitive treatment for AMD exists as yet, but supplementation with antioxidants or minerals (e.g., high doses of vitamins C and E, beta carotene, zinc, lutein, and zeaxanthin) may provide some protective effect or slow the progression to advanced disease in patients with mild AMD.64,65 However, others question the effectiveness of such supplements in AMD.66-70 Surgical and drug delivery treatments have been identified to be successful in slowing or eliminating the progression of AMD. Clinical trials continue to seek improved treatment modalities.

B L O O D S U P P L Y

T O U V E A L T R A C T

The short posterior ciliary arteries enter the globe in a circle around the optic nerve, and their branches form the choroidal vessels. The long posterior ciliary arteries and the anterior ciliary arteries join to form the major circle of the iris, which supplies vessels to the iris and ciliary body. The venous return for most of the uvea is through the vortex veins (see Chapter 11 for further information on the blood supply).

U V E A L I N N E R V A T I O N

Sensory innervation of the uvea is provided through the nasociliary branch from the trigeminal nerve. Sympathetic fibers from the superior cervical ganglion via

FIGURE 3-22

Fundus photo showing right eye of 49-year-old with scattered retinal drusen. (Courtesy Fraser Horn, OD, Pacific University Family Vision Center, Forest Grove, Ore.)

FIGURE 3-23

Fundus photo showing left eye of patient with AMD, confluent drusen, disciform scarring, and pigment mottling in the macular area is evident. (Courtesy Fraser Horn, OD, Pacific University Family Vision Center, Forest Grove, Ore.)

the ophthalmic and short ciliary nerves innervate the choroidal blood vessels, and sympathetic fibers from the superior cervical ganglion via the long ciliary nerves innervate the iris dilator and ciliary muscles. Parasympathetic fibers from the ciliary ganglion innervate the ciliary muscle, the iris sphincter muscle, and the choroidal vessels.

RPE

Bruch’s membrane

FIGURE 3-24

Summary of implications of lipid accumulation in Bruch’s membrane for transport systems operating across retinal pigment epithelium (RPE).  In youngest age group:

1, metabolites pass from choroid through Bruch’s membrane across RPE to neural retina; 2, water moves predominantly from neural retina to choroid; and 3, progress of catabolism results in accumulation of waste products that are predominantly cleared via the choroid. In older age group: 4, with increasing age, catabolism results in accumulations (lipofuscin) within RPE; 5, waste products rich in lipid begin to accumulate within Bruch’s membrane; 6, accumulation of lipid-rich debris within Bruch’s membrane may inhibit metabolic input to neural retina; and

7, presence of a hydrophobic barrier within Bruch’s membrane impedes passage of water and may result in detachment of RPE. (From Pauleikhoff D, Harper CA, Marshall J, et al: Aging changes in Bruch’s membrane: a histochemical and morphological study, Ophthalmology 97[2]:171, 1990.)

A G I N G C H A N G E S

I N U V E A

IRIS

With age, loss of pigment from the epithelium is evident at the pupillary margin and on transillumination. Pigment deposition may be seen on the iris surface, anterior lens surface, posterior cornea, and trabecular meshwork. The dilator muscle becomes atrophic, and the sphincter muscle becomes sclerotic, making it more difficult to dilate the older pupil pharmacologically.71

CILIARY BODY

Although the amount of connective tissue within the layer of ciliary muscle increases with age,72 there is no significant correlation between loss of ciliary muscle contractile ability and age.72,73 Ciliary muscle contraction does not diminish with age.74 The formation of aqueous decreases with age and by age 80 is approximately 25% of what it was; however, the volume of the anterior chamber decreases by about 40%.36