Ischemic retinal vasculitis is frequently seen secondary to tuberculosis and retinal vasculitis associated with tuberculoprotein hypersensitivity. Tuberculous retinal vasculitis is typically an obliterative periphlebitis affecting the retina in multiple quadrants, starting at or anterior to the equator and progressing posteriorly. Occasionally, it can begin close to the optic nerve head, mimicking a vein occlusion. Ophthalmoscopic findings vary and depend on the stage of the disease. Initially, it presents as active retinal periphlebitis with thick exudates around the retinal veins associated with retinal hemorrhages and hemorrhagic infarctions of the retina. Healed periphlebitis results in sclerosed white venules and abnormal vascular anastomosis. The periphlebitis may cause nonperfusion of a substantial portion of the retina that may lead to proliferative vascular retinopathy with sequelae such as recurrent vitreous hemorrhage, traction retinal detachment, rubeosis iridis, and neovascular glaucoma. The management of active tuberculous retinal vasculitis or retinal vasculitis associated with tuberculoprotein hypersensitivity requires the use of systemic steroids and appropriate antituberculous therapy. New vessel formation associated with capillary closure responds to scatter laser photocoagulation. It is important to identify the presence of retinal ischemia in patients with tuberculous retinal vasculitis because scatter laser photocoagulation should be considered when angiographic evidence of widespread retinal nonperfusion is present and before (or shortly after) the development of neovascularization. Early vitrectomy and adequate endolaser photocoagulation should be considered in eyes with non-resolving vitreous hemorrhage associated with active fibrovascular proliferation. Tuberculous retinal vasculitis should be suspected in the presence of florid retinal periphlebitis with marked capillary closure with a relatively mild degree of vitreous cellular infiltrate, particularly in patients of Asiatic origin: Genetic predisposition may account for the propensity to develop retinal vasculitis in these patients. Most patients have no history of pulmonary or other systemic forms making a definitive diagnosis difficult. It should be emphasized that the absence of clinically evident pulmonary tuberculosis (TB) does not rule out the possibility of ocular TB, as about 60 % of patients with extrapulmonary TB have no evidence of pulmonary TB.