Cataracts are a relatively common blinding complication of diabetes mellitus in dogs. The pathophysiology of diabetic cataracts involves a persistent hyperglycemia that overwhelms the lens’ glycolysis pathway, resulting in shunting of glucose into the sorbitol pathway via the enzyme aldose reductase. Sorbitol cannot diffuse out of the lens, thus creating a hyperosmotic effect that leads to swelling. This swelling is associated with alterations in lenticular electrolyte levels, increased membrane permeability, and the formation of water clefts and vacuoles. As this process continues, an irreversible cataract eventually forms. Since the cataracts are often rapid onset with increased lens volume, there is an increased risk of lens capsule leakage, which results in phacolytic uveitis (intraocular inflammation that is induced by lens proteins). Occasionally, the lens capsule can actually rupture, leading to another form of lens-induced uveitis called phacoclastic uveitis. Treatment of cataracts involves surgery, with the most commonly performed procedure being phacoemulsification followed by the implantation of artificial intraocular lenses. Prognosis for sight after treatment is overall very good with atraumatic surgery if there are no active pre-operative secondary complications (i.e. lens-induced uveitis) and if a strict post-operative treatment protocol is followed.