Exposure to ionizing radiation can damage the retinal vasculature. Radiation retinopathy typically has a delayed onset, is slowly progressive, and causes microangiopathic changes that clinically resemble diabetic retinopathy. Radiation retinopathy depends on dose fractionation and can occur after either external-beam or local plaque therapy, typically within months to years after radiation treatment. In general, radiation retinopathy is observed around 18 months after treatment with external-beam radiation and earlier with brachytherapy. Because radiation retinopathy appears very similar to other vascular diseases, eliciting a history of radiation treatment is important in establishing the diagnosis. An exposure to doses of 30–35 grays (Gy) or more is usually required to induce clinical symptoms; occasionally, however, retinopathy may develop after as little as 15 Gy of external-beam radiation. Studies have shown retinal damage in 50% of patients receiving 60 Gy and in 85%–95% of patients receiving 70–80 Gy. The total dose, volume of retina irradiated, and fractionation scheme are important in determining the threshold dose for radiation retinopathy. See BCSC Section 4, Ophthalmic Pathology and Intraocular Tumors, for further discussion of these therapies.
Clinically, affected patients may be asymptomatic or may describe decreased visual acuity. Ophthalmic examination may reveal signs of retinal vascular disease, including cotton-wool spots, retinal hemorrhages, microaneurysms, perivascular sheathing, capillary telangiectasis, macular edema, and optic nerve head edema. Capillary nonperfusion, documented by fluorescein angiography, is commonly present, and extensive retinal ischemia can lead to neovascularization of the retina, iris, or optic nerve head (Fig 7-16). Other possible complications include optic atrophy, central retinal artery occlusion, CRVO, choroidal neovascularization, vitreous hemorrhage, neovascular glaucoma, and tractional retinal detachment. Vision outcome is primarily related to the extent of the macular involvement with CME, exudative maculopathy, or capillary nonperfusion. Occasionally, vision loss may be caused by acute optic neuropathy.
Figure 7-16 Radiation retinopathy. Images of an eye that has undergone plaque brachytherapy for treatment of choroidal melanoma. The melanoma can be seen nasally, obscuring part of the optic nerve head. Typical radiation retinopathy changes are apparent. A, In the fundus photograph, cotton-wool spots, exudates (“hard” exudates), and intraretinal blot hemorrhages are visible. B, The fluorescein angiography image shows microvascular abnormalities (representative of capillary nonperfusion) superior to the fovea and adjacent to an enlarged foveal avascular zone. Additional areas of nonperfusion are noted in the macula and near periphery.
(Courtesy of Tara A. McCannel, MD, PhD.)
Anti-VEGF may be an effective treatment for radiation retinopathy. Laser photocoagulation is less effective because it creates retinal atrophy and laser scar pigment creep.
Patel SJ, Schachat AP. Radiation retinopathy. In: Albert DM, Miller JW, Azar DT, Blodi BA, eds. Albert & Jakobiec’s Principles and Practice of Ophthalmology. 3rd ed. Philadelphia: Saunders; 2008:chap 175.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.