Delhi Journal of Ophthalmology

Radiation Retinopathy with Neo-Vascular Glaucoma

Rishi Sharma, Sandeep Shankar, V.S Gurunadh, Alok Sati
Command Hospital (EC),
Kolkata, West Bengal, India

Corresponding Author:

Rishi Sharma
Command Hospital (EC),
Kolkata
West Bengal, India
Email: rishi4840@yahoo.co.in

Published Online: 13-APR-2015

DOI:http://dx.doi.org/10.7869/djo.124

Abstract

Keywords :

Dear Editor

The tremendous benefits, and dangers, of radiation therapy have been known since at least the 1930s, when radia¬tion became a cornerstone of cancer treatment. Marie Curie, in fact, the revered physicist who conducted the world’s first studies of radioactive isotopes to treat cancer, died in 1934 of aplastic anemia, her demise widely attributed to unshielded work with radiation. Henry Stallard, who pioneered cobalt plaque therapy for pediatric ocular tumors, died of cancer as well. For ocular cancer patients, the effects of radiation secondary to the desired therapeutic ones include cataract, glaucoma and vitreous hemorrhage, as well as radiation retinopathy and maculopathy. The last two are the most common causes of irreversible radiation-related vision loss.[1]

Case Report

We report a case of severe intra-ocular hypoxia following radiotherapy to the adjoining area manifesting as severe intra-ocular neo-vascularisation leading to retinopathy and neovascular glaucoma and managed successfully by pan- retinal photocoagulation (Figure 1 & 2). 31 yrs old male patient presented with painless progressive diminution of vision in left eye of 6 months duration. He initially presented with epistaxis of 9 months duration. He was evaluated and CT scan showed sinonasal growth left side with infiltrates in ethmoid, sphenoid sinuses and orbit. Biopsy showed squamous cell carcinoma in left maxilla. Pt was put on CCRT and received a total of 64 Gray units of radiation. The Best corrected visual acuity was 6/6 in right eye and Counting of fingers close to face (CFCF) in the left eye. The anterior segment and fundus examination was essentially normal in right eye. Left eye examination revealed steamy cornea with florid neovascularisation of angle and the iris. Fundus examination showed Neovascularisation of the Disc (NVD) and multiple areas of neovascularisation elsewhere (NVE). Intraocular pressure (IOP) was 16 mm Hg in the right eye and 50 mm Hg in the left eye by Goldman’s applanation tonometry (GAT). Based on the above findings the patient was diagnosed as a case of Radiation Retinopathy Grade IV with Neo-Vascular Glaucoma (left Eye). He was started on oral and topical anti-glaucoma medications. He underwent 3 sittings of Pan Retinal laser photocoagulation (PRP). The best corrected visual acuity was 6/6 in right eye and CFCF in the left eye. The anterior segment and fundus examination was essentially normal in right eye. In the left eye, the cornea was clear and the NVI had regressed. Relative afferent pupillary defect was present and there was posterior sub capsular cataract. IOP was 16 mm Hg in the right eye and 18 mm Hg in the left eye. Gonioscopic evaluation revealed regressing angle new vessels. The patient has been kept on regular follow up.

Discussion

Radiation retinopathy is a chronic, progressive retinal and papillary vasculopathy induced by suprathreshold doses of ionizing radiation.[2] In 1933, Stallard first described retinal inflammation and degeneration with exudates, hemorrhages, retinal pigment epithelium changes, and optic disc edema in patients treated with radon seeds for retinal tumors.[3] Radiation retinopathy has been reported within seven months and up to 8.5 years after external beam radiation and between four to 32 months after radioactive plaque therapy.[4] Precise incidence is not known but is probably underestimated because many patients with early or mild retinopathy have few or no symptoms and some patients with established disease are so gravely ill that the ocular pathology goes unreported. The key determinants in the development of radiation retinopathy are the total dose of radiation administered to the retina and the fraction size in the case of teletherapy. In brachytherapy for choroidal melanoma or retinoblastoma, local retinal and choroidal changes are universal and the severity of retinopathy is directly proportional to the dose of radiation. Brachytherapy for posterior melanomas, especially within 5mm of the macula, carries a significant risk of maculopathy and loss of vision.[5] The minimum dose of brachytherapy to induce maculopathy is unknown, although one study of brachytherapy for posteriorly located retinoblastomas recorded maculopathy in 7 of 18 eyes that received an estimated macular dose of 6000rad (60Gy) and in 9 of 10 eyes that received a macular dose of 7500rad (75Gy) or more.[6] The threshold dose of teletherapy for clinical retinopathy is also unknown; estimates fall in the range 1500–6000 rad (15–60Gy). The incidence of radiation retinopathy steadily increases with doses greater than 4500 rad (45Gy).[7] Dose fractions, the field design, and the type and rate of administration of radiation also have to be taken into account. A general rule is that patients whose eyes receive radiation doses of less than 2500rad (25Gy) in fractions of 200 rad (2Gy) or less are unlikely to develop significant retinopathy. Increased risk of developing radiation retinopathy in coexisting conditions such as Diabetes, Hypertension, Collagen disorders, Acute leukemias, Concomitant chemotherapy.[8] Retinal vascular endothelial cell is the first and prime casualty of retinal irradiation .ionizing radiation interrupts cell processes during interphase, causing cell death. Focal loss of endothelial cells and pericytes cause weakening of the cell wall leading to the formation of microaneurysms and rupture of microaneurysms results in intraretinal hemorrhages all this results in retinal hypoxia leading to release ofvascular endothelial growth factors (VEGF) resulting in neovascularisation.[9] The earliest clinical features of radiation retinopathy are discrete foci of occluded capillaries and irregular dilatation of the neighboring microvasculature at the posterior fundus. Fluorescein angiography confirms the extent of capillary dropout and the general capillary competence at this stage. As the retinopathy develops, microaneurysms and telangiectatic channels appear particularly in areas of depleted capillaries, and with time become incompetent. Retinal exudation and small intraretinal or nerve fiber hemorrhages may be superimposed on the gradually evolving Ischaemic retinopathy; however, with modest radiation damage the retinopathy and vision may change little over a period of years. More substantial radiation injury is associated with diffuse capillary closure and microvascular incompetence that leads to macular exudation, edema, and decline in vision. An acute form of Ischaemic retinopathy may follow intense retinal irradiation, as in the course of eradicating a nasopharyngeal or orbital tumor, during which eye protection is limited. The clinical picture is one of Ischaemic retinal necrosis with widespread arteriolar occlusion, cotton-wool spots, and superficial and deep retinal hemorrhages, which affect both central and peripheral neural retina.[3] Some resolution of hemorrhage and absorption of axoplasmic debris and edema typically occur, and a very limited reperfusion of Ischaemic areas may be evident. Intraretinal microvascular abnormalities are commonly observed in Ischaemic retinopathy, and, where vascular occlusion is extensive, preretinal and papillary neovascular membranes form. Most patients who have proliferative retinopathy develop the new vessels within 2 years of diagnosis of retinopathy.[11] Vitreous hemorrhage, traction detachment, rubeosis iridis, and phthisis bulbi are end-stage complications of severe radiation damage to the eye. Blurred vision usually results from macular edema or macular ischemia. Blind and painful eye in advanced cases of radiation damage occurs as a result of radiation-induced ocular ischemia or neovascular glaucoma. A history of cephalic radiotherapy and the presence of an Ischaemic retinopathy usually suffice to secure a diagnosis of radiation retinopathy.





Differential diagnosis :- Includes the following
 1.Diabetic retinopathy
 2. Branch retinal vein obstruction
 3. Central retinal vein obstruction
 4. Accelerated hypertensive retinopathy
 5. Coats’ disease
 6. Perifoveal telangiectasia
 7. Ischaemic optic neuropathy
 8 Optic neuritis
 9. Papilledema

Pan-retinal photocoagulation is the modality of treatment and Kinyoun et al reported a success rate of 91% in 11 eyes treated with pan-retinal photocoagulation. Combination Therapy using intravitreal steroids and anti-VEGF agents as anti-VEGF agents decrease leakage and suppress neovascularization, and steroids help resolve inflammation and may stabilize the retinal vasculature. McCannel et al have found that in cadaveric eyes, silicone oil attenuates the radiation absorbed by nontumor tissue by approximately 50 percent. Prognosis: Patients with Non- proliferative retinopathy retain a visual acuity of 6/15(20/50) for at least 4 yrs. Proliferative retinopathy has a very poor prognosis with 86% patients having visual acuity of 20/200 or worse after 6 years. Severe intra-ocular hypoxia following radiotherapy to the adjoining area manifesting as severe intra-ocular neo-vascularisation leading to retinopathy and neovascular glaucoma. Managed successfully by pan- retinal photocoagulation.

Radiotherapy is an essential modality of treatment for tumours; however radiation retinopathy is among the treatment complications when treatment is given to areas adjacent to the eyes. It is important that the ophthalmologist and radiotherapist liaise closely when patients receive cephalic radiation that involves the eye in the treatment field. Careful monitoring of the patient and judicious photocoagulation can help preserve vision in patients who may otherwise be severely disabled for a variety of reasons.

Financial & competing interest disclosure

The authors do not have any competing interests in any product/procedure mentioned in this study. The authors do not have any financial interests in any product / procedure mentioned

References
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Sharma R, Shankar S, Gurunadh VS, Sati ARadiation Retinopathy with Neo-Vascular Glaucoma.DJO 2015;25:283-285

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Sharma R, Shankar S, Gurunadh VS, Sati ARadiation Retinopathy with Neo-Vascular Glaucoma.DJO [serial online] 2015[cited 2020 Mar 31];25:283-285. Available from: http://www.djo.org.in/articles/25/4/radiation-retinopathy.html