The crystalline lens is composed of specialized cells arranged in a highly ordered manner. Lens epithelial cells have a very high content of crystallin protein that imparts transparency to the lens. Unlike other epithelial cells, lens epithelial cells are not shed and are particularly susceptible to the degenerative effects of aging. Photo-oxidative insult has been shown to play an important role in the pathogenesis of cataract. The vast majority of cataracts occur in the elderly and reflect senescent change. Risk factors associated with acquired cataract in developed nations include age, smoking, alcohol consumption, sunlight exposure, diabetes, and systemic or topical corticosteroid use. Other causes of cataract include ocular trauma, lead exposure, uveitis, and radiation for intraocular tumor. Certain systemic diseases, such as myotonic dystrophy, Wilson disease, Down syndrome, and other metabolic diseases, are also associated with increased risk of cataract formation.

Cataracts are painless and progress slowly; formation is typically bilateral, although it is often asymmetrical. Patients with visually significant cataracts usually complain of problems with night driving, reading road signs, or difficulty with fine print. Other symptoms include monocular diplopia and an increase in nearsightedness (“myopic shift”). Age-related cataract typically has three components: nuclear sclerosis, cortical spoking, and posterior subcapsular haze. Each affects a different part of the lens and has different symptoms and progression, although the indication for intervention with all types is the same.

Nuclear sclerotic cataracts progress very slowly and occur commonly with age. Continued production of lens fibers causes hardening and compression of the lens nucleus. As lens proteins aggregate, the refractive index and transparency of the lens shift and the lens becomes yellowish brown (i.e., “brunescent”). The first visual consequence of nuclear sclerotic cataract formation is often a shift toward nearsightedness because of the increased refractive index and thickness of the sclerotic nucleus. Visual impairment is initially more marked at distance than near, and a patient may fail a driver’s license examination and still be able to read a newspaper. Eventually, as the nucleus becomes more opaque, visual clarity diminishes at all distances. Patients are often unaware of the gradual spectral change causing a yellow cast to the visual world; they usually acknowledge it only after the cataract is removed. Loss of contrast sensitivity may cause functional impairment out of proportion to the results of a standard high-contrast visual acuity test.

Cortical cataracts develop when the more peripheral lens fibers opacify in a spokelike pattern. These spokelike opacities often cause glare due to the scattering of light entering the eye. Glare can be quite significant, leading to difficulties with night driving well before a loss of visual acuity.

Posterior subcapsular cataracts form at the back of the lens, usually centrally. The central location of the opacity causes the vision to worsen when the pupil is small, as in reading or in bright light. The refractile nature of the opacity commonly causes severe glare, especially when driving at night. Pupillary dilation with mydriatic or cycloplegic drops or with use of subdued light improves vision in such cases, as images may reach the retina around the cataract. Although occasionally helpful, this therapy is not usually a long-term solution. This type of cataract is often responsible for the “presenile” cataract seen in the 40- to 50-year-old age group. Posterior subcapsular cataracts are associated with prolonged use of topical, inhaled, or systemic steroids and with diabetes mellitus.

Traumatic cataracts can result from any type of ocular trauma, penetrating or nonpenetrating. Penetrating injuries may perforate the lens capsule, allowing the lens protein to hydrate and thereby denature and opacify or damage the metabolic processes of lens resulting in diffuse opacification. Electric shock and high-dose ionizing radiation may lead to lens opacification.

Initial evaluation by the primary physician includes visual acuity determination both near and at a distance. The lenticular opacity can be appreciated with the direct ophthalmoscope while attempting to visualize the fundus. If the angle is not shallow, dilation with one drop of 2.5% phenylephrine or 1% tropicamide is
helpful. With the ophthalmoscope lens set at zero and standing about 12 inches from the patient, a bright red reflex is seen in the normal eye. Cataract formation is clearly seen by the disruption of the red reflex. Plus power (black numbers) in the ophthalmoscope of about 15 or 20 diopters will put the lens of the eye in focus as the physician approaches the eye. The fundus should be examined for retinal abnormalities, particularly macular degeneration (manifested by hemorrhage, scarring, and drusen), which can cause a loss of vision symptomatically similar to that from cataract. In all cases of visual impairment, an ophthalmic consultation is indicated.