Ophthalmic considerations The ocular effects of irradiation depend not only on total dose, fractionation, and treatment portal size but also on the presence of any associated systemic diseases such as diabetes mellitus and hypertension. Concomitant chemotherapy has an additive effect.

The lens is the most radiosensitive structure in the eye, followed by the cornea, the retina, and the optic nerve. The orbit is completely included in the treatment portal in diseases such as large retinoblastomas; it is partially included in tumors of adjacent structures, such as the maxillary antrum, nasopharynx, ethmoid sinus, and nasal cavity. Usual radiation doses range from 20 to 100 Gy. The total dose is usually fractionated into smaller doses during the treatment. In brachytherapy, a low-energy isotope such as radioactive iodine delivers a high dose of radiation within a few millimeters of the tumor but does not penetrate deep into it. This allows for radioactive episcleral implants to deliver a dose of 100 Gy to the apex of a tumor but a much lower dose to the rest of the eye. The sclera can tolerate doses up to 400–800 Gy.

Doses to the lens as low as 2 Gy in a single fraction may cause cataract formation. However, cataracts caused by low doses may be asymptomatic and may not progress. Cataracts resulting from higher doses (7–8 Gy) may continue to progress, resulting in considerable vision loss. The average latent period for the development of radiation-induced cataracts is 2–3 years.

The clinical picture of radiation retinopathy resembles that of diabetic retinopathy. The usual interval between radiation therapy and the development of radiation-induced retinopathy is 2–3 years. Radiation retinopathy may develop earlier in patients with diabetes mellitus or in those undergoing chemotherapy. The earliest clinical manifestation of radiation retinopathy is usually cotton-wool spots. After several months, these spots fade away, leaving areas of capillary nonperfusion. Telangiectatic vessels grow from the retina into these areas. Microaneurysms may also develop. These ischemic changes may cause neovascularization of the iris, which in turn may lead to neovascular glaucoma. The capillary endothelial cell is the first type of cell to be damaged, followed closely by the pericytes and then the endothelial cells of the larger vessels. The new intraretinal telangiectatic vessels have thick collagenous walls. There may be spotty occlusion of the choriocapillaris. Panretinal photocoagulation or injection with anti–vascular endothelial growth factor (anti-VEGF) agents are effective treatments for radiation retinopathy. See BCSC Section 12, Retina and Vitreous, for more on this topic.

Radiation optic neuropathy may present with optic nerve head pallor with splinter hemorrhages. Injury to the more proximal part of the optic nerve resembles retrobulbar optic neuropathy. Affected patients may report unilateral headaches and ocular pain; the optic nerve head may not reveal edema or hemorrhage. With doses of 60–70 Gy, dry eye syndrome sometimes develops. This syndrome usually develops within a year and occasionally progresses to corneal ulceration and severe pain. For more on radiation optic neuropathy, see BCSC Section 5, Neuro-Ophthalmology.

Ocular manifestations of fetal irradiation in the first trimester include microphthalmos, congenital cataracts, and retinal dysplasia.