Glaucoma and vitreoretinal surgeries have long been associated with cataract progression. 1-10 There have been many theories to explain this phenomenon. These theories include direct or indirect mechanical damage from instrumentation, light toxicity from the operating scope, intraocular irrigating solution, use of intraocular gas, intraocular inflammation, and advanced patient age. 11,12 These theories, however, do not distinguish between the different types of cataracts that form postoperatively, nor do they provide a unified coherent explanation for the observed cataract progression. In this chapter, we propose a mechanism of cataractogenesis, specifically nuclear sclerosis formation, which we believe occurs as a function of altered aqueous fluid dynamics after intraocular surgery. We present this as the nutrient theory of cataractogenesis.Before detailed discussion of the nutrient theory of cataractogenesis as a function of altered aqueous fluid dynamics, a background review of the following concepts will serve as a vital conceptual framework for its understanding: 1) anatomy and metabolism of the lens, 2) aqueous humor and vitreous biochemistry, 3) fluidics of the aqueous humor and vitreous, 4) types of cataracts, 5) recognized causes of cataracts, and 6) current theories of nuclear sclerosis formation after pars plana vitrectomy.
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