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A 38-year-old male drug abuser had multiple emboli in the retinal circulation of the posterior pole of both eyes. He showed widespread peripheral retinal capillary nonperfusion and neovascular proliferation at the junction of perfused and nonperfused retina. The emboli were considered to be talc particles from the intravenous administration of suspensions of oral medications. The presumed mechanism of development of neovascularization in this case was the filtering out of the particles by the retinal vasculature with vaso-occlusion, ischemia and subsequent retinal neovascularization.
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