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104 Clinical Anatomy of the Visual System

A posterior subcapsular cataract is a disturbance located just beneath the posterior capsule (Figure 5-15). This type of cataract impacts vision early and significantly given its location along the visual axis and near the nodal point of the eye. A significant risk factor for posterior subcapsular cataracts is long-term, highdose steroid use.

Clinical Comment: Cataract Surgery

The decision for cataract removal is determined by the effect the cataract has on the patient’s everyday life. When a person is not able to perform the usual daily activities because of reduced vision caused by the opacity, the lens should be removed. Cataract extraction is a relatively safe surgical procedure usually done under local anesthesia. A small incision is made to allow entrance

of surgical instruments into the anterior chamber. The anterior lens capsule is opened and the lens epithelium and all fibers are removed, with the lens capsule remaining intact. An intraocular lens (IOL) can then be inserted into the lens capsule to replace the power of the missing lens. Multifocal IOLs that correct for presbyopia may be an option.

The Physiology of Cataract Formation

Numerous mechanisms are presumed causative for cataracts, including fluid and ion imbalance, oxidative damage, protein modification, and metabolic disruption.66 A disturbance in fluid regulation can be caused by ionic pump dysfunction and/or membrane permeability increase that allows water accumulation. If Na+/K+ ATPase pump activity decreases significantly, a rise in Na+ in the cytoplasm is accompanied by an influx of water, the lens fibers swell and transparency diminishes.69 An increased level of cytoplasmic Ca++ is also associated with a loss of transparency.69 Water accumulation between fibers can form vacuoles causing a disruption of fiber arrangement and increased light scatter. UVR and oxidative damage as a result of free radical accumulation affects cellular function, damages lens DNA, causes protein modification, and high-molecular-weight crystallin aggregations, any of which can increase light scatter.25 Alpha crystallins, as molecular chaperones, help to stabilize beta/gamma crystallin configuration but by age 40 have disappeared from the lens nucleus, although the normal lens usually remains fairly transparent for years past that age.92 But as the concentration of alpha crystallins is reduced, aggregates accumulate and with time form light-scattering opacities.

Glutathione and ascorbate maintain a reducing environment providing some protection from free radical damage and preventing protein modification. Reduced levels of glutathione allow oxidative damage to membranes and proteins.77 A decrease in glutathione

FIGURE 5-12

Grading system for age-related cataracts.  Nuclear sclerotic changes are shown in cross section, with anterior surface to the left. Cortical and posterior subcapsular changes are seen in retroillumination. (From Fingeret M, Casser L, Woodcome HT: Atlas of primary eyecare procedures, Norwalk, Conn, 1992, Appleton & Lange.)

concentration is associated with cataract development.92,93 A barrier, speculated to develop in middle age and located at the interface of the cortex and nucleus, seems to impede the flow of small molecules from the cortex into the nucleus and might account for the reduction in glutathione in the nucleus.91 A modification of the connexins in gap junctions causes a disruption in communication between fibers and might be one cause of this barrier.94,95 Changes occur in aquaporin channel proteins in the innermost nuclear regions of the lens as early as age 5 and by middle age (age 40 to 50), half of such channels are lost in the region of the speculated barrier.82 These changes can lead to the occlusion of the water channels and contribute to the barrier function.

A diabetic cataract results from elevated glucose levels and can develop rapidly. With increased blood glucose, excess glucose present in the aqueous enters

CHAPTER 5  t  Crystalline Lens 105

A B

FIGURE 5-13

Nuclear cataract seen with A, diffuse illumination, and B, optic section. (From Kanski JJ, Nischal

KK: Ophthalmology: clinical signs and differential diagnosis, St Louis, 2000, Mosby.)

FIGURE 5-14

Spokes of a cortical cataract visible against the red reflex. (Courtesy Pacific University Family Vision Center, Forest Grove, Ore.)

the lens. As this excess glucose is metabolized, sorbitol accumulates faster than it is converted to fructose. Sorbitol concentration increases within the lens fiber, because sorbitol does not readily pass through the fiber membrane, and thus water is drawn into the fiber. The fibers swell, the lens loses transparency, and the fibers may eventually rupture.

Age-Related Cortical Cataract

High lifetime exposure to UVR is associated with increased incidence of cortical cataracts; the paradox is that the most severe damage in cortical cataracts occurs near the equator initially, the area most protected from sunlight by the iris. Cortical cataracts are associated with increased membrane permeability and ion transporters, pumps, and exchangers are not able to maintain the

FIGURE 5-15

Posterior subcapsular cataract. (From Kanski JJ, Nischal KK:

Ophthalmology: clinical signs and differential diagnosis, St Louis, 2000, Mosby.)

homeostatic concentration.71 An increased concentration of Ca++ in the fiber cytoplasm also drives fluid accumulation.69 Affected regions of the fiber show disruption of structure and can include membrane rupture. The changes first occur in the center of the elongated fiber (that is at the equatorial region), with the apical and basal ends remaining transparent. Generally the tapered fiber ends, located at the sutures in the optical axis, are only affected very late in the life of the cortical cataract.

Age-Related Nuclear Cataract

Age-related nuclear cataracts are associated with a decline of glutathione, making the fibers susceptible to oxidative damage. Levels can be significantly reduced in the nucleus while levels in the cortex remain within the normal range.78,94 Oxidative protein modification increases significantly after age 50, contributing to the damage