The Pathology of Cataracts - Cataract Surgery, 3rd Edition

Cataract Surgery, 3rd Edition

PART I – Evaluation

Chapter 1 – The Pathology of Cataracts

Terrence S. Spencer, MD,
Nick Mamalis, MD

Contents

	•	Lens Embryology
	•	Normal Anatomy Of The Lens
	•	Introduction To Cataract Pathology
	•	Congenital Cataracts
	•	Nuclear Cataracts
	•	Cortical Cataracts
	•	Posterior Subcapsular Cataracts
	•	Anterior Subcapsular Abnormalities
	•	Traumatic Cataracts
	•	Pseudoexfoliation And True Exfoliation
	•	Conclusion

CHAPTER HIGHLIGHTS

		Development of the lens
		Pathologic correlation of clinical cataracts

Lens embryology

Knowledge of the embryology of the lens helps one better understand its normal anatomy and the nature of cataracts. Lens cells form early during embryogenesis from surface ectoderm. The optic vesicles (neuroectodermally derived outpouchings of the diencephalon) enlarge to come in contact with the surface ectoderm which thickens to form the lens plate. At the same time, the optic vesicle begins invaginating and an indentation called the lens pit forms in the lens plate. The lens pit continues to invaginate as surface ectoderm cells multiply. Eventually, a sphere of cells called the lens vesicle breaks off from the stalk which kept it connected to the remainder of the surface. The lens vesicle at this point contains a single layer of cuboidal cells within an outer basement membrane. The outer basement membrane forms the lens capsule.

The posterior cells of the lens vesicle begin to elongate anteriorly to become the primary lens fibers (Figure 1-1). These primary lens fibers meet the anterior lens cuboidal cells, obliterating the lumen of the lens vesicle. The primary lens fibers make up the embryonic nucleus, and the anterior lens cuboidal cells are now referred to as the lens epithelial cells. The layer of lens epithelium maintains its presence anteriorly and just posterior to the equator, but no epithelial cells are normally present in the posterior part of the lens.



Figure 1-1 Embryo lens. Posterior epithelial cells of the lens vesicle elongate to become lens fibers. (Hematoxylin and eosin [H & E] stain; X10.)

Secondary lens fibers form from lens epithelial cells near the equator, which begin to multiply and elongate anteriorly under the lens epithelium and posteriorly under the lens capsule. These secondary lens fibers form the fetal nucleus during gestation and continue to grow in this manner adding new layers. As the lens fibers grow, they extend from the equator to meet anteriorly and posteriorly, forming Y-shaped sutures where they meet during fetal growth. During childhood and early adolescence, lens fibers surround the fetal nucleus to become the juvenile or infantile nucleus. Further growth of these lens fibers eventually forms the adult nucleus. Subsequent lens fibers grow to surround the entire nucleus, forming lens cortex.

During fetal development the lens nucleus becomes enveloped within the tunica vasculosa lentis, a nutritive support structure supplied by the hyaloid artery. This structure atrophies and usually disappears by birth.

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Normal anatomy of the lens

The lens is normally a clear, biconvex structure (Figure 1-2). Viewed from the side, it has an elliptical shape, measuring about 3.5–4.0 mm A–P by 9.0–10.0 mm in diameter. It is located posterior to and loosely apposed to the iris. Lens transparency is a function of regular cell shape, regular cell volume, minimal extracellular space, and minimal scatter elements.^[1]



Figure 1-2 Normal lens. This histologic section of a normal lens from an enucleated globe showing artefactual clefts and folds. (Hematoxylin and eosin [H & E] stain; X2.)

The lens is held in place by the zonules, which attach it to the ciliary body. The zonular fibers arise from the basement membrane of the non-pigmented epithelium of the ciliary body and attach just anteriorly and posteriorly to the equator of the lens. Tension on the zonules is reduced by contraction of the ciliary muscle, allowing the lens to become more spherical in shape for accommodation.

The lens is lined on its outer surface by the lens capsule, which is responsible for elasticity, allowing the lens to accommodate. The lens capsule varies in thickness and is thinnest at the posterior pole. Histologically, the lens capsule stains positive with PAS stain since it is a true basement membrane of the lens epithelial cells.

Lens epithelial cells are arranged in a single row of cuboidal cells along the anterior surface of the lens and ending at the lens bow where new lens fibers are produced. Nutrients and waste products pass through the lens capsule by diffusion and active transport from the anterior epithelium. The equatorial bow region of the lens (Figure 1-3), just posterior to the equator, is where lens epithelial cells elongate to form lens fiber cells. Normally, there are no lens epithelial cells along the posterior pole of the lens capsule.



Figure 1-3 Lens bow. Lens epithelial cells elongate from the equator to form new lens fibers. The nuclei appear to "fan out" from the edge of the lens seen in cross section. There are no epithelial cells beneath the posterior surface of the lens capsule. (Hematoxylin and eosin [H & E] stain; X10.)

The cortex and nucleus make up the substance of the lens. The fibers derived earliest lie centrally and form the embryonic, fetal, juvenile and, finally, adult nucleus. The lens cortex is formed from the most peripheral fibers found between the nucleus and capsule (Figure 1-4). As more cortical fibers are produced at the periphery, inner fibers are added to the defined adult lens nucleus.



Figure 1-4 Lens substance. Normal fibers appear in layers at the periphery of the lens. The clefts are artifacts from histologic sectioning. (Trichrome stain; X20.)

Studies of the morphology of differentiated lens fiber cells in all regions of normal adult human lenses have been performed.^[2] The percentages of the lens thickness that is accounted for by the embryologic nucleus was found to be 4%, this was followed by 49% of the lens thickness made up of the fetal nucleus, 9% juvenile nucleus, 21% adult nucleus and, lastly, 17% the cortex. Evaluation of the morphology of lens fibers by electron microscopy showed that the cells in the embryonic and fetal nucleus were rounded with variable area. Adult nuclear cells were found to be more flattened with a relatively intricate, membranous interdigitation. Cortical cells evaluated by electron microscopy were irregularly hexagonal in shape.

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Introduction to cataract pathology

The term cataract refers to any opacity of various degree of the crystalline lens, which is normally almost completely transparent. There are a variety of methods to classify cataracts clinically, but pathological examination of cataracts may be difficult. The lens tends to survive fairly well post-mortem because it does not have its own blood supply, but it does not have the same gross appearance as its clinical appearance in vivo. Hardness of the explanted lens correlates highly with clinical grading of nuclear sclerosis, but not with cortical or subcapsular opacities.^[3,][4] One problem with pathological examination of a cataract is the alteration in the appearance of the lens when it is placed in fixatives for the purpose of preservation of tissue. The microscopic alterations that are seen on histologic sections do not necessarily correlate with the severity of cataract and visual dysfunction seen clinically. When the lens is processed and sectioned for histologic examination, numerous artefacts appear in its structure.

With normal aging, the lens increases in overall size and loses its ability to accommodate. Continued growth of lens fibers with aging causes the nucleus to become compressed and less pliable (nuclear sclerosis).^[3,][5] Nuclear lens proteins aggregate and are chemically modified to produce pigmentation, decreasing transparency. The increase in pigmentation causes the lens nucleus to appear yellow, or with excess pigmentation, brown (brunescent cataract). Proteins within the cytoplasm of lens cells are modified in such a manner that scatters visible light, resulting in opacification.^[6] A decrease in metabolic transport of antioxidants in an aging lens, as a consequence, may allow oxidation of nuclear components.^[7]Hydrogen peroxide (H₂O₂), one oxidant, is found at elevated concentrations in some patients with maturity-onset cataract. The activities of glutathione peroxidase, the major enzyme which metabolizes H₂O₂, and other antioxidant enzymes may be reduced in older individuals.^[8] The oxidative damage is thought to start in the nucleus of the lens where metabolic activities would be lowest and where modified proteins, susceptible to oxidation, would accumulate with age.^[9]

Changes within the lens nucleus are usually accompanied by changes in other parts of the lens. Aging causes nuclear, cortical, and posterior subcapsular cataracts, each to varying degrees. When these changes cause a cataract in the lens, the patient may experience visual impairment, loss of contrast, dulling perception of color, and may also become increasingly myopic. In addition to loss of visual acuity, cataract development may be associated with visual abberations such as monocular double or triple vision.^[10] Clinically mature or “ripe” cataracts may result in total opacification and liquefaction. A hypermature or “overripened” cataract sometimes progresses from the stage of morgagnian cataract (see below) to a shrunken membranous cataract after spontaneous loss of liquid protein and resorption of liquefied cortex.

Cataracts are clinically classified in different manners according to location, age of onset, appearance, or cause. The other sections of this book will thoroughly cover the etiology of cataracts related to disease and medications. At this point we will focus our chapter primarily on the histopathologic features of cataracts based mainly on location of the cataract within the lens.

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Congenital cataracts

Congenital cataracts are present at birth or noted shortly afterwards. The morphology of congenital cataracts can be helpful in establishing their etiology and prognosis.^[11] They are usually bilateral and may occur in association with other medical problems. The insult to the developing lens is often mild enough that the resultant opacity does not interfere with vision.

Congenital zonular cataracts are characterized by opacities situated in one layer of the lens and surrounded by clear lens. A central nuclear cataract from an insult early in development of the lens would be displaced deeper into the lens substance as new fibers grow throughout life.^[12] An embryonal nuclear cataract results from an injury to the lens during the first 2 months of gestation and would be seen as a small central opacification. A fetal nuclear cataract (Figure 1-5) results from an insult at about the 3rd month of gestation and would lie between the level of the anterior and posterior Y-sutures or at the sutures (sutural cataract). Sutural opacities with secondary arborization or branching signify a teratologic insult later in gestation. A perinuclear or lamellar zone from a later insult would be arranged concentrically to the lens capsule with the cataractous layer surrounding the nucleus. The lamellar cataract takes its name from the laminar or sheet-like anatomy of the lens and is surrounded by the more peripheral clear cortical layers of the lens.^[13,][14]



Figure 1-5 Fetal nuclear cataract. Clinical appearance of a central cataract surrounded by normal lens tissue.

Polar cataracts are opacities located on the anterior or posterior pole. Fibrous metaplasia of the anterior lens epithelium causes an anterior polar cataract (Figure 1-6). When caused by hyperplasia of the embryonal pupillary membrane, a conical mass of connective tissue (pyramidal cataract) protrudes into the anterior chamber. Histologically, a localized loss of epithelial cells with an anterior subcapsular plaque is seen (see also anterior subcapsular cataract later in this chapter).



Figure 1-6 Anterior polar cataract. The lens epithelium has been replaced by fibrous metaplasia. (Hematoxylin and eosin [H & E] stain; X20.)

A posterior polar cataract is a larger disc-shaped opacity resulting from persistent hyperplastic primary vitreous, and can result in degeneration of the posterior subcapsular cortex with progressive opacification. A hyaloid vessel remnant, called a Mittendorf dot, is a small, dense white spot on the posterior surface of the lens and is clinically insignificant.

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Nuclear cataracts

The most common age-related opacity of the lens is the nuclear sclerotic cataract (Figure 1-7). Increased compaction of nuclear fibers in age-related cataracts may be a contributing factor for excessive scatter in nuclear opacification.^[15] Clinically, cataractous lens nuclei have decreased transparency in addition to the increased amount of pigmentation often found in normal aging. The lens nucleus normally appears histologically to have cellular laminations, which become more compact with aging. Lenses with nuclear sclerotic cataracts are characterized histopathologically by subtle changes with a dense homogeneous appearance (Figure 1-8). The laminations fade, and the nucleus becomes amorphous, taking on a more uniform eosinophilic staining characteristic. In an isolated nuclear sclerotic cataract, the surrounding cortical fibers would microscopically retain visible outlines of the cytoplasmic membranes. The increase in lens pigmentation seen clinically is not usually evident by histopathologic examination, but crystalline deposits are sometimes observed.^[16]



Figure 1-7 Cataractous lens. This enucleated globe is sectioned sagittally to show the gross appearance of a cataractous lens.



Figure 1-8 Nuclear sclerotic cataract. The nucleus from this post-mortem globe with a senile cataract takes on a dense homogenous appearance. Changes are often subtle, as in this specimen. (Trichrome stain; X2.)

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Cortical cataracts

Aging changes in the lens cortex result in cortical cataracts. Cortical cataracts begin with relatively sharp clear fluid clefts which result in opaque spokes or can have more clear lamellar separations resulting in cuneiform-type opacities.^[17] Lens epithelium likely plays a role in the loss of transparency of the cortex.^[18] Insoluble proteins are assumed to be characteristic of cortical cataractous epithelium, which is also accompanied by various morphological abnormalities such as spokes or rosettes (Figure 1-9A, B).^[19] Histopathologically, accumulation of eosinophilic fluid between lens cells with displacement and degeneration of bordering cells characterize cortical cataracts (Figure 1-10). Clefts seen microscopically correspond to visible changes observed clinically by slit-lamp examination. Spherical droplets or globules of released protein from the breakdown of cortical cell walls are calledmorgagnian globules (Figure 1-11). Encountering these droplets during surgical cataract excision may release milky fluid. These globules may accumulate and may eventually replace the entire cortex and result in a mature morgagnian cataract.^[20] The central dense nucleus at this point would become gravity dependent often displaced inferiorly to the lower equatorial region of the lens (Figure 1-12).



Figure 1-9 Cortical cataract. A, Clinical photograph of a senile cataract with cortical fluid clefts. B, Posterior view of an enucleated globe with cortical spokes.



Figure 1-10 Cortical cataract. Histologic section of an early cortical cataract with accumulation of eosinophilic fluid between lens fibers. (Hematoxylin and eosin [H & E] stain; X10.)



Figure 1-11 Morgagnian globules. Advanced cortical cataract with breakdown of lens proteins, histologically appearing as eosinophilic-staining spheres. (Hematoxylin and eosin [H & E] stain; X10.)



Figure 1-12 Morgagnian cataract. Gross appearance of a dense lens nucleus and its associated capsule in a mature morgagnian cataract.

The deep cortex of some lenses has been found to have crystalline deposits, which can appear as a “Christmas-tree cataract.”^[21] The crystals may be formed from cholesterol, lipids, calcium, or other compounds and in many cases does not decrease visual acuity unless other forms of cataracts coexist, but these crystals can be associated with phacolytic glaucoma.^[22] Some forms of crystals are visible on histologic examination by use of cross-polarized filters.

In addition to various biochemical changes which may be related to the formation of cortical cataracts, physical forces must also be considered. An increase in nuclear lens hardening may lead to disaccommodation in older lenses which can theoretically develop mechanical sheer stresses between the soft cortex and the hard nuclei. These sheer stresses may be significant in the different cortical ruptures with a radial direction of sharply limited choroidal spokes or parallel micro-ridges at the area of lamellar separations which may explain some of the histopathologic changes seen in cortical cataracts. Various mechanical sharp limited cortical ruptures are caused by a combination of predisposing and sheer forces. The sheer forces occur during disaccommodation between the soft outer and the increasingly harder central lens layers.^[17]

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Posterior subcapsular cataracts

Clinically visible opacification located just anterior to the posterior lens capsule may be formed idiopathically or after an injury to the posterior area of the lens. In addition, posterior subcapsular cataracts may form secondary to multiple medications, such as corticosteroids, and in association with various systemic conditions. These posterior subcapsular cataracts appear as focal dot-like granular areas or plaques in the posterior subcapsular cortex (Figure 1-13). This type of cataract is associated with degeneration of subcapsular posterior cortical cells followed by proliferation of peripheral lens epithelial cells, which migrate posteriorly beyond the lens bow at which it normally terminates.^[23] The posterior migration of lens epithelial cells possibly represents an attempt to replace the degenerate, sometimes liquefied, lens substance in the cataractous lens and can be seen in diverse cataract conditions. The abnormally positioned epithelial cells enlarge and are called bladder or Wedl cells.^[24] The nuclei of the bloated bladder cells are visible in histologic sections (Figure 1-14).



Figure 1-13 Posterior subcapsular cataract. Clinical photograph of a focal granular area in the posterior subcapsular cortex.



Figure 1-14 Bladder cells (Wedl cells). Lens epithelial cells have become swollen after abnormally migrating to the posterior pole of the lens. (Hematoxylin and eosin [H & E] stain; X20.)

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Anterior subcapsular abnormalities

Subepithelial lens opacities have been observed following an attack of acute glaucoma, and, when such an association exists, are described as Glaukomflecken. The severe elevation of intraocular pressure may form grayish opacities localized beneath the anterior lens capsule, which histologically appear as focal areas of epithelial cell necrosis.^[25] Epithelial cell degeneration can be in response to other insults, such as radiation and inflammation.

An anterior subcapsular plaque can form from proliferation and subsequent degeneration of lens epithelial cells leading to opacities. This type of cataract is usually the result of irritation, from uveitis, or disruption from trauma (discussed later in this chapter). Histologically, the plaque of the anterior or equatorial lens epithelium appears as a thin layer of fibrous tissue (fibrous metaplasia).^[26] Multiple layers of such plaques may be laid down with intervening layers of normal cortex to form a reduplication cataract (Figure 1-15).



Figure 1-15 Anterior subcapsular cataract. Epithelial cells appear posterior to an abnormal fibrous plaque. (Hematoxylin and eosin [H & E] stain; X20.)

Anterior subcapsular cataracts have an accumulation of extracellular matrix that also contains lens epithelial cells which have fibroblast-like appearances. Studies of these various matrix components reveal them to be comprised of collagen, fibronectin, and fibrillin, as well as multiple different growth factors which may be responsible in helping to either signal or activate the lens epithelial cells in these types of cataracts.^[27]

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Traumatic cataracts

Contusion of the eye may be severe enough to cause deposition of iris pigment on the lens capsule (Vossius ring). A Vossius ring is an imprint of the pupillary margin of the iris, and the pigment may resolve with time. Severe enough blunt force may cause formation of a cataract, which initially appears stellate with opacities lying in the cortex or capsule. Disruption of the lens zonular fibers due to injuries can cause the lens to be dislocated or partially dislocated (subluxated). Some blunt traumas cause both cataract formation and dislocation of the lens. The dislocation may be in any direction. Changes leading to lens opacity in traumatic cataracts appear to involve epithelial and subsequent cortical fiber deterioration.^[28] In a contusion-type injury to the lens, traumatically induced dysfunction of lens epithelium may lead to edema of the superficial cortical lens fibers that subsequently undergo degeneration and produce a localized and permanent lamellar zone of vacuolization. With time and the formation of new clear lens cells, this layer becomes gradually compressed and displaced deeper into the cortex.^[29]

Laceration or perforation of the lens capsule from trauma results in a localized opacity usually progressing to opacification of the entire lens. Histologically, the ruptured capsule typically appears as a wrinkled membrane. Opacities from small capsular injuries may remain stable as a focal cortical cataract, but exposed cortex often swells, expanding through the capsular tear. This process may induce a granulomatous inflammatory response of the remaining lens nucleus. Retained metallic foreign bodies within the lens may cause focal rusty appearing opacities (siderosis lentis).

The lens is susceptible to damage induced by ionizing radiation, with cataract formation often occurring many years after the initial exposure. Cataracts induced by radiation are usually observed in the posterior region of the lens, often in the form of a posterior subcapsular cataract.^[30] There is a cumulative effect to radiation exposure of the lens, but large doses can cause sudden injury to lens epithelial cells and subsequent opacity of the entire lens. Infrared radiation and intense heat exposure to the lens, as seen in glass blowers, has caused cobweb-like cortical opacities and changes in the lens capsule.

When only a small portion of lens epithelial cells and cortical material remain in the periphery of the capsule following trauma or cataract extraction, a Soemmerings' ring cataract may form (Figure 1-16). The epithelial remnants undergo proliferation or fibrous metaplasia to form a doughnut-shaped ring. A histologic examination of the Soemmerings' ring would reveal a barbell-shaped cross-section with a residual lens capsular membrane forming the shaft that connects a bulbous prominence of retained lens cortex at one or both equators^[31] (Figure 1-17).



Figure 1-16 Soemmerings' ring cataract. The Soemmerings' ring in this eye formed after traumatic rupture of the capsule and loss of most of the lens contents. (Hematoxylin and eosin [H & E] stain; X2.).



Figure 1-17 Soemmerings' ring cataract. Lens epithelial cells proliferate in the periphery of the lens capsule. (Trichrome stain x 40.)

Lens epithelial cells displaced through the capsule by accidental or surgical trauma can regenerate and proliferate in an abnormal location to form Elschnig pearls. Microscopically, the pearls resemble clusters of the bladder cells (Wedl cells) found in the posterior aspect of a cataractous lens, except they are found in the anterior chamber on the lens surface or iris stroma.

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Pseudoexfoliation and true exfoliation

Exfoliation syndrome (pseudoexfoliation) is a different entity to true exfoliation.^[32] True exfoliation is a rare delamination of the lens capsule, which peels off in outward curling scrolls. Most patients with true exfoliation have a history of exposure to intense heat or infrared radiation. Histologically, the lens capsule appears thickened, and the outer portion may peel away from the intact layer closest to the lens epithelium. The peripheral portion of lens capsule often appears normal.^[33]

In contrast, the more common pseudoexfoliation material is believed to be basement membrane material arising within the anterior chamber and appearing on the lens, iris, corneal endothelium, and trabecular meshwork. The material, initially believed to be a deposit on the lens,^[32] is synthesized from lens epithelial cells, and by cells of the iris and ciliary epithelium.^[34] Clinically, the deposit appears on the anterior lens capsule as a central disc surrounded by a relatively clear zone, surrounded by peripheral granular area. Pseudoexfoliation can cause secondary open-angle glaucoma called glaucoma capsulare. Weakening of the zonular fibers can complicate cataract surgery in these patients. Histopathologically, the lens capsule surface appears to have straight deposits resembling iron filings aligned on a magnet (Figure 1-18). The material may also be found on or within the iris, trabecular meshwork, and the corneal endothelium.



Figure 1-18 Pseudoexfoliation. This curled up piece of anterior lens capsule removed during cataract surgery shows deposits lined up resembling iron filings on a magnet. The outer surface of the lens capsule is opposite the remaining lens epithelial cells. (Hematoxylin and eosin [H & E] stain; X100.)

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Conclusion

In conclusion, cataracts can present with a large variety of histopathologic changes. These cataractous changes can involve any of the structures of the lens including the nucleus and the cortex, as well as anterior and posterior subcapsular areas. A thorough understanding of the pathology of various types of cataracts will allow the surgeon to more adequately prepare for the removal of a cataractous lens.

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References

[1]. Garner M.H., Kuszak J.R.: Cations, oxidants, light as causative agents in senile cataracts. P R Health Sci 1993; 12:115-122.

[2]. Taylor V.L., Al-Ghoul K.J., Lane C.W., et al: Morphology of the normal human lens. Inv Oph & Vis Sci 1996; 37:1396-1410.

[3]. Heyworth P., Thompson G.M., Tabandeh H., McGuigan S.: The relationship between clinical classification of cataract and lens hardness. Eye 1993; 7:726-730.

[4]. Assia E.I., Medan I., Rosner M.: Correlation between clinical, physical, and histopathological characteristics of the cataractous lens. Graefes Arch Clin Exp Ophthalmol 1997; 235:745-748.

[5]. Duncan G., Wormstone I.M., Davies P.D.: The aging human lens: structure, growth, and physiological behaviour. Br J Ophthalmol 1997; 81:818-823.

[6]. Clark J.I., Clark J.M.: Lens cytoplasmic phase separation. Int Rev Cytol 2000; 192:171-187.

[7]. Truscott R.J.: Age-related nuclear cataract: a lens transport problem. Ophthalmic Res 2000; 32:185-194.

[8]. Spector A.: Oxidation and aspects of ocular pathology. J CLAO 1990; 16:S8-10.

[9]. Augusteyn R.C.: Protein modification in cataract: possible oxidative mechanisms. In: Duncan G., ed. Mechanisms of cataract formation in the human lens, London: Academic Press; 1981:72-111.

[10]. Campbell C.: Observations on the optical effects of a cataract. J Cataract Refract Surg 1999; 25:995-1003.

[11]. Lambert S.R., Drack A.V.: Infantile cataracts. Surv Ophthalmol 1996; 40:427-458.

[12]. Eagle R.C.J., Spencer W.H.: Lens. In: Spencer W.H., ed. Ophthalmic pathology: an atlas and textbook, vol. 1. 4th ed.. Philadelphia: WB Saunders Company; 1996:372-437.

[13]. Grottrau P.D., Schlotzer-Schrehardt U., Dorfler S., Naumann G.O.H.: Congenital zonular cataract: clinicopathologic correlation with electron microscopy and review of literature. Arch Ophthalmol 1993; 111:235-239.

[14]. Potter W.S.: Pediatric cataracts. Ped Clin North Am 1993; 40:841-851.

[15]. Al-Ghoul K.J., Nordgren R.K., Kuszak A.J., Freel C.D., Costello M.J., Kuszak J.R.: Structural evidence of human nuclear fiber compaction as a function of aging and cataractogenesis. Exp Eye Res 2001; 72:199-214.

[16]. Zimmerman L.E., Johnson F.B.: Calcium oxalate crystals within ocular tissues. Arch Ophthalmol 1958; 60:372-383.

[17]. Pau H.: Cortical and subcapsular cataracts: significance of physical forces. Ophthalmologica 2006; 220:1-5.

[18]. Worgul B.V., Merriam G.R.J., Medvedovsky C.: Cortical cataract development – an expression of primary damage to the lens epithelium. Lens Eye Toxic Res 1989; 6:559-571.

[19]. Kalariya N., Rawal U.M., Vasavada A.R.: Human lens epithelial layer in cortical cataract. Indian J Ophthalmol 1998; 46:159-162.

[20]. Bron A.J., Habgood J.O.: Morgagnian cataract. Trans Ophthalmol Soc UK 1976; 96:265.

[21]. Shun-Shin G.A., Vrensen G.F.J.M., Brown N.P.: Morphologic characteristics and chemical composition of Christmas tree cataract. Invest Ophthalmol Vision Sci 1993; 34:3489-3496.

[22]. Flocks M., Litwin C.S., Zimmerman L.E.: Phacolytic glaucoma: a clinicopathologic study of one hundred thirty-eight cases of glaucoma associated with hypermature cataract. Arch Ophthalmol 1955; 54:37.

[23]. Eshaghian J., Streeten B.W.: Human posterior subcapsular cataract, An ultrastructural study of the posteriorly migrating cells. Arch Ophthalmol 1980; 98:134-143.

[24]. Wedl C. Atlas der pathologischen Histologie des Auges. Leipzig: Wigand; 1860–1861.

[25]. Anderson D.R.: Pathology of the glaucomas. Br J Ophthalmol 1972; 56:146-157.

[26]. Font R.L., Brownstein S.: A light and electron microscope study of anterior subcapsular cataracts. Am J Ophthalmol 1974; 78:972-984.

[27]. Ishida I., Saika S., Okada Y., Ohnishi Y.: Grown factor deposition in anterior subcapsular cataract. J Cataract Refract Surg 2005; 31:1219-1225.

[28]. Rafferty N.S., Goossens W., March W.F.: Ultrastructure of human traumatic cataract. Am J Ophthalmol 1974; 78:985-995.

[29]. Asano N., Schlotzer-Schrehardt U., Dofler S., Naumann G.O.H.: Ultrastructure of contusion cataract. Arch Ophthalmol 1995; 113:210-215.

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Contents

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Cataract Surgery, 3rd Edition

PART I – Evaluation Chapter 1 – The Pathology of Cataracts

PART I – Evaluation

Chapter 1 – The Pathology of Cataracts