against lens protein. The inflammation may follow accidental or surgical trauma to the lens. Histologically, lens-induced granulomatous endophthalmitis consists of a central nidus of

degenerating lens material surrounded by concentric layers of inflammatory cells (zonal granuloma). Multinucleated giant cells and neutrophils are present within the inner layer adjacent to degenerating lens material. Lymphocytes and plasma cells make up the intermediate mantle of cells. These cells may be surrounded by fibrovascular connective tissue, depending on the duration of the inflammatory response (Figs 9-4, 9-5). See also BCSC Section 9, Intraocular Inflammation and Uveitis.

Phacolytic Glaucoma

See Chapter 7 for a discussion of this topic.

Propionibacterium acnes Endophthalmitis

Chronic postoperative endophthalmitis secondary to P acnes may develop following cataract surgery, usually 2 months to 2 years later. Onset of the inflammation may follow Nd:YAG laser capsulotomy that allows release of the sequestered organisms. Propionibacterium acnes endophthalmitis can present with granulomatous keratic precipitates, a small hypopyon, vitritis, and a white plaque containing bacteria and residual lens material sequestered within the capsular bag (Figs 9-6, 9-7).

Degenerations

Cataract and Other Abnormalities

Capsule

Mild thickening of the lens capsule can be associated with pathologic proliferation of lens epithelium or with chronic inflammation of the anterior segment. Elements with an affinity for basement membranes, such as copper (chalcosis) and silver (argyrosis), can form pigmented deposits in the anterior lens capsule.

Epithelium

A severe elevation of intraocular pressure causes injury to the lens epithelial cells, leading to degeneration of the cells. Clinically, patches of white flecks (glaukomflecken) are seen beneath the lens capsule. Histology shows focal areas of necrotic lens epithelial cells beneath the anterior lens capsule. Associated degenerated subepithelial cortical material is also present. See also BCSC Section 10, Glaucoma.

Injury to the lens epithelium can also be caused by inflammation, ischemia, or trauma and can stimulate epithelial hyperplasia and formation of anterior subcapsular fibrous plaques (Fig 9-8A). In this situation, the epithelial cells have undergone metaplastic transformation into fibroblast-like cells, which are capable of producing collagen. These functionally transformed epithelial cells arise in response to a variety of stimuli, including inflammation, ischemia, and trauma. Following resolution of the inciting stimulus, the lens epithelium may produce another capsule, thereby completely surrounding the fibrous plaque and producing a duplication cataract (Fig 9-8B).

Retention of iron-containing metallic foreign bodies in the lens may lead to lens epithelial degeneration and necrosis, secondary to siderosis. The presence of iron within the epithelial cells can

be demonstrated by Perls Prussian blue stain.

Posterior subcapsular cataract may be the most common abnormality involving the lens epithelium. There are a number of risk factors for this condition, including chronic intraocular inflammation, diabetes mellitus, ionizing radiation exposure, smoking, and prolonged corticosteroid use (Fig 9-9A; see Fig 9-8A). Posterior subcapsular cataract is frequently associated with cortical degeneration and nuclear sclerosis. Histologically, development of this type of cataract begins with epithelial disarray at the equator, followed by posterior migration of the lens epithelium. As the cells migrate posteriorly, they enlarge and swell to 5–6 times their normal size. These swollen cells, referred to as bladder cells of Wedl, can cause significant visual impairment if they involve the axial portion of the lens (Fig 9-9B).

Disruption of the lens capsule often results in proliferation of lens epithelial cells. Following extracapsular cataract extraction, for example, remaining epithelial cells can proliferate and cover the inner surface of the posterior lens capsule, producing clinically appreciable posterior capsule opacification. These collections of proliferating epithelial cells may form partially transparent globular masses, called Elschnig pearls, which are histologically identical to bladder cells of Wedl (Fig 9-10). Sequestration of proliferating lens fibers in the equatorial region, often as a result of incomplete cortical removal during cataract surgery, may create a doughnut-shaped configuration referred to as a Soemmering ring cataract (Fig 9-11).

Cortex

Opacities of the cortical lens fibers are most often associated with nuclear sclerosis, posterior subcapsular cataracts, and ultraviolet light exposure. Clinically, cortical degenerative changes fall into 2 broad categories: generalized discolorations with loss of transparency and focal opacifications.

Generalized loss of transparency cannot be diagnosed histologically with reliability, as histologic stains that are used to colorize the lens after it is processed prevent the assessment of lens clarity. The earliest sign of focal cortical degeneration is hydropic swelling of the lens fibers with decreased intensity of the eosinophilic staining. Focal cortical opacities become more apparent when fiber degeneration is advanced enough to cause liquefactive change. Light microscopy shows the accumulation of eosinophilic globules (morgagnian globules) in slitlike spaces between the lens fibers, which is a reliable histologic sign of cortical degeneration (Fig 9-12; see Fig 9-13C). As focal cortical lesions progress, the slitlike spaces become confluent, forming globular collections of lens protein. Ultimately, the entire cortex can become liquefied, allowing the nucleus to sink downward and the capsule to wrinkle (morgagnian cataract) (Fig 9-13).

Denatured lens protein can escape through an intact lens capsule and provoke an anterior chamber macrophagic inflammatory reaction, a condition known as phacolytic glaucoma (discussed in Chapter 7).

Nucleus

The continued production of lens fibers subjects the nucleus in the adult lens to the lifelong stress of mechanical compression. This compression causes hardening of the lens nucleus. Aging is also associated with alterations in the chemical composition of the nuclear fibers. The pathogenesis of nuclear discoloration is poorly understood and probably involves more than 1 mechanism, including accumulation of urochrome pigment. Clinically, the lens nucleus may appear yellow, brunescent, or deep brown (Fig 9-14).

Nuclear cataracts are difficult to assess histologically because they take on a subtle homogeneous eosinophilic appearance. The loss of cellular laminations (artifactitious clefts) probably correlates better with firmness of the nucleus than it does with optical opacification clinically (Fig 9-13C). Occasionally, crystalline deposits, identified as calcium oxalate, may be observed within a nuclear