Contributor: Gordon K. Klintworth
In iris neovascularization a fibrovascular membrane covers the normally avascular anterior surface of the iris flattening it. This abnormal layer contains myofibroblasts and thin-walled blood vessels. The new blood vessels lack the thick collagenous sheath that typifies normal iris vessels. In long standing iris neovascularization corneal endothelial cells occasionally migrate onto the iris where they produce a hyaline membrane comparable to Descemet membrane. Most examples of iris neovascularization accompany retinal neovascularization [neovascularization - retina] and retinoblastoma. Less common causes include chronic retinal detachment, intraocular tumors, chronic intraocular inflammation [endophthalmitis - chronic], ischemia from carotid artery insufficiency and carotid cavernous fistula. Iris neovascularization frequently develops or worsens in persons with diabetes mellitus after cataract extraction, presumably because this removes a physical barrier to the anterior diffusion of a retinal derived angiogenic factor.
One complication of iris neovascularization is neovascular glaucoma [glaucoma - neovascular]. This occurs because the fibrovascular membrane extends into the anterior chamber angle causing peripheral anterior synechiae, which obstruct the trabecular meshwork. The fibrovascular tissue also exerts traction on the pigmented epithelium of the iris causing ectropion uveae. The friable new vessels on the iris readily bleed causing hyphema. Sometimes the abnormal vascularized tissue occludes the pupil.