23.1 Features
While clinical findings of radiation retinopathy and diabetic retinopathy (DR) overlap considerably, a discussion of the initiating insults can provide a better understanding of the disease process. Ionizing radiation induces killing of tumor cells through two general mechanisms: (1) DNA disruption in rapidly proliferating cells and (2) oxidative damage by reactive oxygen species (ROS). A secondary consequence of this process is the collateral damage sustained by local healthy tissue, creating the foundation for the development of radiation retinopathy. In brachytherapy, the dose prescription target volume is defined by the apex of the tumor and a small margin of retina (~ 2 mm) surrounding the tumor base to account for any undetectable tumor extension and imprecision with plaque placement. Retinal regions that fall outside of this area typically have very minimal radiation exposure. Proton beam radiotherapy (PBT) has theoretical advantages over brachytherapy for treating difficult-to-reach posterior tumors as well as minimizing radiation exposure beyond the treatment zone, a phenomenon termed the Bragg peak. External beam radiotherapy (EBT) exposes the entire fundus to radiation, thus this modality can produce radiation retinopathy over a greater area of retina if radiation dosage is not adjusted appropriately. DNA disruption induces degeneration of both endothelial cells and neuroglia, a cell that is critical to support retinal neurons through myelination, homeostasis, and nutrition. Endothelial cells are particularly susceptible to ROS damage from their exposure to high amounts of oxygen and iron within the blood. Furthermore, arteries are affected more than veins due to the higher oxygen tension of arterial circulation. This is in direct contrast to DR, which initially affects pericytes instead of endothelial cells. Patients with concurrent diabetes mellitus are at a higher risk for developing aggressive radiation retinopathy from increased susceptibility given the underlying vascular damage.
23.1.1 Common Symptoms
Early or mild retinopathy may be asymptomatic; more advanced disease can present with decreased vision or floaters.
23.1.2 Exam Findings
Initially microaneurysms, intraretinal hemorrhages, lipid exudation, and leakage of serous fluid into the surrounding tissues maybe seen (▶ Fig. 23.1). Larger retinal vessels become affected later in the disease course and occlude, leading to a progressive vasculopathy with detrimental effects on numerous fundus structures. Susceptibility to developing radiation retinopathy and subsequent response to various treatment modalities varies greatly among patients.
Fig. 23.1 Progression of radiation retinopathy after treatment of choroidal melanoma. (a–c) Early on in the disease course, there is extensive lipid exudation surrounding the tumor lesion as well as mild vascular attenuation and peripapillary cotton wool spots. (d) As disease progresses, proliferative retinopathy results in vitreous hemorrhage due to neovascularization. (e–f) Advanced stages of the disease include sclerosis of retinal vessels leading to vascular nonperfusion and contributing to proliferative disease elsewhere in the retina.
Similar to DR, radiation retinopathy can be further differentiated into subtypes: nonproliferative radiation retinopathy (NPRR), proliferative radiation retinopathy (PRR), and radiation macular edema (RME). Common findings of NPRR include peripheral retinal vascular changes, intraretinal hemorrhages, retinal telangiectasia, retinal exudates, and cotton wool spots. PRR arises from advanced disease inducing large areas of retinal capillary nonperfusion and neovascularization of the retina and optic disc (▶ Fig. 23.2). Uncontrolled PRR can eventually lead to neovascular glaucoma, vitreous hemorrhage, and traction retinal detachment.
Fig. 23.2 Proliferative radiation retinopathy. (a) Fundus image of peripapillary choroidal melanoma treated with radiation resulting in lipid exudation (white arrows), intraretinal hemorrhaging (dashed white arrow), and choroidal neovascularization of the optic disc (black arrow). (b) Red free fundus imaging highlights macular retinal neovascularization (white arrows).
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