Posterior subcapsular opacity

Pilocarpine therapy should be avoided in certain patients (Box 10-10).This drug is contraindicated in patients with cataract, especially nuclear sclerotic and posterior subcapsular cataract, because the drug can affect vision and may accelerate the formation of lens opacities. Pilocarpine is generally contraindicated in patients younger than 40 years of age because of the intolerable accommodative spasm and refractive changes. Because breakdown of the blood-aqueous barrier occurs with the use of pilocarpine and other miotics, particularly in the presence of neovascular and uveitic glaucoma, pilocarpine should be avoided in these patients. 

Topical ocular steroid administration also may cause the development of cataracts in both children and adults. Use of topical steroids for several years to eliminate redness associated with contact lens wear resulted in PSC formation as well as glaucoma and visual field loss. The opacities associated with steroid administration resemble those produced by ionizing radiation and ocular disease such as uveitis, retinitis pigmentosa, and retinal detachment. They differ from opacities associated with diabetes and trauma but are indistinguishable from lens changes associated with posterior subcapsular age-related cataract. 

A 42-year-old Japanese woman received busulfan 212mg/day for only 4 days and developed reduced visual acuity and blurred vision in both eyes she had a posterior polar subcapsular opacity in the lenses in both eyes (14). 

A 49-year-old man with chronic myelogenous leukemia developed dense posterior subcapsular cataracts and punctate cortical opacities after taking busulfan for 5 years (15). Ultrastructural examination showed cortical liquefaction, with Morgagnian droplets involving primarily the region from the equator to the posterior subcapsular space, crystalloid rays, and abundant degenerate lens fiber membranes. 

Deprivation of nutritional compounds and induced metabolic defects. Tryptophane deficiency in the diet causes the rapid formation of a posterior subcapsular cataract (Buschke, 1943). The model has the disadvantage, however, that a concomittant corneal opacity is induced which prevents further lens observation. The corneal opacity disappears again when returning to normal chow, such that the deprivated diet and a normal chow have to be fed in intervals. 

In week 8, slight subcapsular opacities were detected in the anterior lens, too. Up to week 15, these posterior lens opacities progressed rapidly to moderate or severe cortical and nuclear cataracts (Figures 3-4) in all animals (Figure 11). 

S. J. Crews, Posterior subcapsular lens opacities in patients on long-term corticosteroid therapy, Br... 

R.D. Sperduto and R. Hiller, The prevalence of nuclear, cortical and posterior subcapsular lens opacities in a general population sample, Ophthalmol. 91 815(1984). 

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