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Radiation retinopathy
ELSEVIER
Clinical Eye and Vision Care 8 (1996)119-l 22
Specialarticle
Radiation retinopathy Mary Jo Homaybv * , Sabre D. Ayers’ aEye Clinic, Veterans Administration Medical Center, 1100 N. College, Fayetteville, AR 72703, USA bAdjunct Faculty, Northeastern State University College of Optometry, USA ‘Veterans Administration Medical Center, Fayetteville, AR 72703, USA
Abstract Therapeutic radiation to the eye, or in close proximity to the eye, can result in damage to the retina. Manifestations of radiation retinopathy include: intraretinal hemorrhages, hard exudates, macular edema, cotton wool spots, microaneurysms, telangiectatic vessels,sheathed retinal vessels,retinal capillary non-perfusion, or neovascularization. Factors that influence the development of radiation retinopathy are discussed and a case report which includes radiation retinopathy in the differential diagnosis is presented. Keywords:
Radiation retinopathy; Radiation therapy; Chemotherapy; Multiple myeloma
1. Introduction
In 1933, Stallard first reported retinal complications following radiation therapy. He noted retinal vascular changes, as well as optic nerve head swelling and optic atrophy in patients who were treated with radon seed implantation for retinal capillary hemangiomas and retinoblastomas [ll. Radiation therapy is commonly used to treat cancer patients and radiation retinopathy may develop following treatment with either local or external beam radiation directed in or around the eye. Two methods of radiation therapy are available; external beam radiation (teletherapy) and local radiation (brachytherapy), the choice of which is dependent upon the cancer type and location. For example, external beam radiation might be used to treat intracranial tumors, while cobalt plaque therapy, a form of local therapy, may be useful for select orbital tumors [2]. The incidence of radiation retinopathy is dependent upon the dose of radiation, the number and size of radiation fractions, and the total time elapsed
*Corresponding author. Tel.: + 1 501 4434301.
during a course of treatment [31. The concomitant use of chemotherapy and/or the coexistence of diabetes increases the risk of radiation retinopathy [4]. External beam radiation is usually given in 200-300 cGy (centigray-a unit of absorbed radiation abbreviated cGy) fractions daily over l-2 months for a total dose of 3500-7200 cGy [5]. Daily dosage fractions greater than 250 cGy may lead to greater damage [6,7]. Radiation retinopathy is most commonly seen at cumulative doses over 3000-5000 cGy, but has been noted with as little as 1200-1500 cGy [2,8]. Retinopathy ranges from 50% in patients who have received 6000 cGy up to 85-95% in those patients who have been treated with 8000 cGy [61. External beam radiation usually produces more severe retinopathy at lower doses when compared to local therapy 191. Time to onset of retinopathy after radiation therapy varies. Patients may develop retinopathy as early as 6 months after radiation therapy, but the onset may be delayed as much as 3 years [91. The average time of onset for retinopathy after external beam radiation is 18-19 months and following local radiation is 14-15 months [51. The retina, as well as other central nervous system tissues, appears to be quite
0953~4431/96/$15.000 1996ElsevierScienceIreland Ltd. All rights reserved PII:SO953-4431(96)00165-S
resistant
to radiation
120
M.J. Horn,
SD. Ayers
/Clinical
damage [lo]. However, when the retina is affected, the inner layers are more susceptible to damage than the outer layers. The retinal blood vessels are one of the first structures damaged by the radiation. This vascular damage, retinal capillary occlusion resulting from capillary endothelial cell damage, is the hallmark of radiation retinopathy [6]. The precise cellular events leading to capillary occlusion are not fully understood. A scattered population of endothelial cells and, to a lesser degree pericytes, in the capillary walls are thought to be damaged with radiation exposure. The surviving cells may be insufficient to maintain normal capillary function. Vessel damage and increased blood flow secondary to capillary occlusion may lead to the formation of microaneurysms and a telangiectatic-like appearance that is considered pathognomonic for radiation retinopathy [ 111. Clinical features of radiation retinopathy include: intraretinal hemorrhages, hard exudates, cotton wool spots, microaneurysms, telangiectatic vessels, and sheathed retinal vessels (Table 1) [2,5,10]. Eyes exposed to external beam radiation tend to demonstrate more hemorrhages and cotton wool spots, while the local radiation therapy eyes exhibit more exudative changes [5]. The extensive exudative changes seen in local therapy are thought, in part, to be caused by vascular leakage of the intraocular neoplasm [5]. Retinal capillary non-perfusion may vary from minimal to widespread [12]. Neovascularization of the retina or the disc may develop as a sequelae of extensive capillary nonperfusion [5]. Neovascularization of the iris and angle can also ensue. Visual impairment resulting from radiation retinopathy ranges from minimal, to total loss of sight. Decreased vision associated with radiation retinopathy can be attributed to macular nonperfusion, macular edema or exudation, vitreous hemorrhage, neovascular glaucoma, or radiation optic neuropathy [13]. Visual loss related to macular non-perfusion is irreversible, but grid laser photocoagulation may be used to treat macular edema. Panretinal laser photocoagulation is administered for retinal, disc, or iris neovascularization in an attempt to prevent vitreous hemorrhage, tractional retinal detachment, and/or neovascular glaucoma [ 131.
Table 1 Differential
diagnosis of radiation retinopathy
Diabetic retinopathy Hypertensive retinopathy HIV retinopathy Blood dyscrasias Ocular ischemic syndrome
Eye and Vision
Care 8 (1996)
119-122
2. Case report
A 50-year-old Caucasian male presented to the Eye Clinic with a chief complaint of decreased vision in both eyes. The patient had been diagnosed with multiple myeloma for 3 years. The patient’s status was 21 months post autologous bone marrow transplant for IgG Kappa stage III multiple myeloma. In preparation for the transplant, the patient underwent total body irradiation (TBI) of 150 cGy, twice daily for 3 days, totalling 900 cGy. Concurrent with the radiation therapy, chemotherapy was administered consisting of 3.5 mg/kg busulfan daily for 4 days, and 60 mg/kg cyclophosphamide for 2 days. The year preceding the transplant the patient was on a chemotherapeutic regimen. An 18-month remissive state followed his transplant, chemotherapy, and radiation therapy. Unfortunately, the multiple myeloma recurred, again requiring treatment. Current treatment consists of a chemotherapy combination of melphalan 10 mg/prednisone 100 mg daily for 4 days of every month. Recent testing indicates remission, thus treatment may soon be discontinued. Ocular examination revealed best corrected visual acuities (BVA’s) of 20/20-l OD and 20/20 OS with subtle posterior subcapsular cataract (PSC) changes in both eyes. Pupils, intraocular pressures, confrontation fields, extraocular muscles, and all anterior segment findings were normal. Dilated fundus examination revealed cotton wool spots, microaneurysms, and exudates within, and immediately outside, the arcades of both eyes. Over the next five months, BVA’s decreased to 20/25 OD, 20/40 OS, presumably due to progression of the PSC OS more than OD. No other changes in ocular health were noted. The retinal findings in both eyes remained stable and unrelated to the vision loss. 3. Discussion Multiple myeloma is a plasma cell dyscrasia [14] that stems from bone marrow precursor cells [15]. These bone marrow cells initiate malignant proliferation of plasma cells which are specific for production of particular immunoglobulins. Plasma cell tumors most often produce IgG, but may produce IgA, IgD, or IgE. Recommended therapy for multiple myeloma includes combination chemotherapy and radiation therapy resulting in a decrease of myeloma protein production in roughly 75-80% of cases. With treatment, the average post-diagnosis survival time is approximately 2-3 years [15].
M.J. Horn,
SD. Ayers
/Clinical
Eye and Vision
Retinopathy can be caused by multiple myeloma exclusive of radiation therapy. Patients with retinopathy associated with multiple myeloma typically exhibit decreased hemoglobin concentration and platelet counts. A small percentage of patients with multiple myeloma have been noted to have fundus changes consisting of Roth’s spots, flame-shaped hemorrhages, and/or nerve fiber layer infarcts due to the anemia and thrombocytopenia caused by the disease. Less commonly, neovascularization, venous occlusions, and vitreous hemorrhages have been reported in patients with multiple myeloma and associated serum hyperviscosity. These fundus changes are reported to resolve in half of the patients who are treated [15]. In assessing the fundus findings in our patient, the differential diagnosis included diabetes mellitus, hypertension, the human immunodeficiency virus (HIV), pharmacologically induced anemia, ocular manifestations of multiple myeloma, and radiation retinopathy (Table 2). Blood glucose levels, blood pressure assessments, complete blood counts, and an HIV ELISA test were all negative, thus eliminating diabetes, hypertension, pharmacologically-induced anemia, and HIV from the differential. The patient has undergone systemic treatment for approximately 3 years and has normal complete blood counts, indicating that the retinopathy present is unlikely secondary to multiple myeloma. The patient received radiation doses considered to be within safe limits by current radiation therapy guidelines [16], thus ocular protection was not deemed necessary. In addition to his radiation therapy, the patient was also treated with chemotherapy. Patients who are treated with combination chemotherapy and radiation are much more likely to develop retinopathy [5,16]. Radiation therapy and chemotherapy do not have to be administered concomitantly in order to cause this effect [3]. The patient was treated before, during, and after radiation therapy with a variety of chemotherapeutic agents, therefore radiation retinopathy cannot be excluded from the differential diagnosis. The patient was not diabetic, but there is a known synergism between diabetes and radiation retinopaTable 2 Retinal-vascular findings of radiation retinopathy Intraretinal hemorrhages Hard exudates Cotton wool spots Microaneurysms Telangiectatic vessels Sheathed retinal vessels Capillary non-perfusion Neovascularization of retina and/or Diffuse atrophy of RPE
Care 8 (I 996) 119-122
121
thy. Diabetes and radiation appear to affect the retinal capillaries in a similar way [4]. This may help explain the exacerbation of radiation retinopathy in patients with diabetes. We assume that chemotherapeutic agents also have an adverse affect on capillaries, and this might help to explain the increase in radiation retinopathy observed with radiation and chemotherapy in combination. Fortunately, the patient’s retinopathy does not appear to have had a deleterious affect on his vision. The patient’s vision loss in this case is likely related to development of posterior subcapsular cataracts in both eyes. The accelerated cataract development is assumed to be secondary to the prednisone use [17], or to the radiation exposure [18,19,20]. 4. Summary The potential for radiation retinopathy should be considered in the differential diagnosis of retinalvascular anomalies (Table 2). Radiation retinopathy has been reported in association with radiation treatment for such conditions as: ocular neoplasm, thyroid disease, tumors of the central nervous system, tumors of the paranasal sinuses [lo], and tumors of the face and lids [13]. A thorough case history may help identify patients with prior radiation treatments that have the potential to cause ocular manifestations. Determining the dose, number and size of radiation fractions, and the total time of radiation treatment is helpful in assessing a patient’s risk for developing retinopathy. Other risk factors should also be evaluated in patients who have been treated with radiation. Chemotherapy administered in association with radiation increases the chances of retinopathy, as does diabetes. Additionally, it is important to determine if the eyes were shielded during radiation therapy. Shielding the eye during radiation therapy may help prevent damage to the eye. A full ocular health examination is important in a post radiation patient. Additional diagnostic testing may also be necessary, such as fluorescein angiography to diagnose macular non-perfusion. Finally, patients should be educated regarding the possible development of retinopathy associated with their disease and/or treatment and the need for appropriate follow-up. References [t]
ONH
Stallard HB. Glioma retinae treated by radon seeds. Br J Med 1936;962-964. [2] Lopez PF, Stemberg P, Dabbs CK, Vogler WR, Cracker I, Alin NS. Bone marrow transplant retinopathy. Am J Ophthalmol 1991;112:635-646..
122 [31 [41
151
b1 [71
Bl [91
DO1
[ill
M.J. Horn,
SD. Ayers
/Clinical
Chacko DC. Considerations in the diagnosis of radiation injury. J Am Med Assoc 1981;245:1255-1258. Viebahn M, Barricks ME, Oserioh MD. Synergism between diabetic and radiation retinopathy: case report and review. Br J Ophthalmol 1991;75:629-632. Brown GC, Shields JA, Sanbom G, Augsburger JJ, Savino PJ, Schatz NJ. Radiation retinopathy. Ophthalmology 1982; 89:1494-1501. Harris JR, Levene MB. Visual complications following irradiation for pituitary adenomas and craniopharyngiomas. Radiology 1976;120:167-171. Aristizabal S, Caldwell WL, Avila J. The relationship of the time dose fractionation factors to the complications in the treatment of pituitary tumors by irradiation. Int J Radiat Oncol Biol Phys 1977;2:6667-673. Quinn AG, Clemett RS. Retinopathy after low-dose retinal irradiation. Aust N Z J Ophthalmol 1993;21(3):193-197. Brown GC. Radiation retinopathy. In: Duane’s Clinical Ophthalmology. Philadelphia, J.B. Lippincott, 1991. Nakissa N, Rubin P, Strohl R, Keys H. Ocular and orbital complications following radiation therapy of paranasai sinus and review of literature. Cancer malignancies 1983;51:980-986. Archer DB, Amoaku WMK, Gardiner TA. Radiation retinopathy clinical, histopathological, ultrastructural and experimental correlations. Eye 1991;5:239-251.
Eye and Vision
Care 8 (1996)
119-122
Amoaku WMK, Archer DB. Fluorescein angiographic features, natural course and treatment of radiation retinopathy. Eye 1990;4:657-667. 1131 Schachat AP. Radiation retinopathy. In: Retina: Vol.11. St. Louis, C.V. Mosby Co., 1989. Knapp AJ, Gartner S, Henkind P. Multiple myeloma and its D41 ocular manifestations. Ophthalmology 1987;31:343-351. 1151 Lukes RJ, Collins RD. Tumors of the hematopoetic system. Bethesda, MD, Armed Forces Institute of Pathology, 1992130-137. Ml Gordon KB, Char DH, Sager-man RH. Late effects of radiation on the eye and ocular adnexa. Int J Radiat Oncol Biol Phys 119;31:1123-1139. 1171 Shalka HW, Prchal JT. Effect of corticosteroids on cataract formation. Arch Ophthalmol 1980;98:1773-1777. 1181 Pitts DG, Kleinstein RN. Environmental vision: interactions of the eye, vision, and the environment. Boston, Butterworth Heinemann, 204-206. Hayes BP, Fisher RF. Influence of a prolonged period of D91 low-dosage X-rays on the optic and ultrastructural appearances of cataract of the human lens. Br J Ophthalmol 1979;63:457-464.
1201 Bray LC, Carey PJ, Proctor SJ, Evans RGB, Hamilton PJ. Ocular complications of bone marrow transplantation. Ophthalmol 1991;75:611-614.
Br J
Clinical Eye and Vision Care 8 (1996)119-l 22
Specialarticle
Radiation retinopathy Mary Jo Homaybv * , Sabre D. Ayers’ aEye Clinic, Veterans Administration Medical Center, 1100 N. College, Fayetteville, AR 72703, USA bAdjunct Faculty, Northeastern State University College of Optometry, USA ‘Veterans Administration Medical Center, Fayetteville, AR 72703, USA
Abstract Therapeutic radiation to the eye, or in close proximity to the eye, can result in damage to the retina. Manifestations of radiation retinopathy include: intraretinal hemorrhages, hard exudates, macular edema, cotton wool spots, microaneurysms, telangiectatic vessels,sheathed retinal vessels,retinal capillary non-perfusion, or neovascularization. Factors that influence the development of radiation retinopathy are discussed and a case report which includes radiation retinopathy in the differential diagnosis is presented. Keywords:
Radiation retinopathy; Radiation therapy; Chemotherapy; Multiple myeloma
1. Introduction
In 1933, Stallard first reported retinal complications following radiation therapy. He noted retinal vascular changes, as well as optic nerve head swelling and optic atrophy in patients who were treated with radon seed implantation for retinal capillary hemangiomas and retinoblastomas [ll. Radiation therapy is commonly used to treat cancer patients and radiation retinopathy may develop following treatment with either local or external beam radiation directed in or around the eye. Two methods of radiation therapy are available; external beam radiation (teletherapy) and local radiation (brachytherapy), the choice of which is dependent upon the cancer type and location. For example, external beam radiation might be used to treat intracranial tumors, while cobalt plaque therapy, a form of local therapy, may be useful for select orbital tumors [2]. The incidence of radiation retinopathy is dependent upon the dose of radiation, the number and size of radiation fractions, and the total time elapsed
*Corresponding author. Tel.: + 1 501 4434301.
during a course of treatment [31. The concomitant use of chemotherapy and/or the coexistence of diabetes increases the risk of radiation retinopathy [4]. External beam radiation is usually given in 200-300 cGy (centigray-a unit of absorbed radiation abbreviated cGy) fractions daily over l-2 months for a total dose of 3500-7200 cGy [5]. Daily dosage fractions greater than 250 cGy may lead to greater damage [6,7]. Radiation retinopathy is most commonly seen at cumulative doses over 3000-5000 cGy, but has been noted with as little as 1200-1500 cGy [2,8]. Retinopathy ranges from 50% in patients who have received 6000 cGy up to 85-95% in those patients who have been treated with 8000 cGy [61. External beam radiation usually produces more severe retinopathy at lower doses when compared to local therapy 191. Time to onset of retinopathy after radiation therapy varies. Patients may develop retinopathy as early as 6 months after radiation therapy, but the onset may be delayed as much as 3 years [91. The average time of onset for retinopathy after external beam radiation is 18-19 months and following local radiation is 14-15 months [51. The retina, as well as other central nervous system tissues, appears to be quite
0953~4431/96/$15.000 1996ElsevierScienceIreland Ltd. All rights reserved PII:SO953-4431(96)00165-S
resistant
to radiation
120
M.J. Horn,
SD. Ayers
/Clinical
damage [lo]. However, when the retina is affected, the inner layers are more susceptible to damage than the outer layers. The retinal blood vessels are one of the first structures damaged by the radiation. This vascular damage, retinal capillary occlusion resulting from capillary endothelial cell damage, is the hallmark of radiation retinopathy [6]. The precise cellular events leading to capillary occlusion are not fully understood. A scattered population of endothelial cells and, to a lesser degree pericytes, in the capillary walls are thought to be damaged with radiation exposure. The surviving cells may be insufficient to maintain normal capillary function. Vessel damage and increased blood flow secondary to capillary occlusion may lead to the formation of microaneurysms and a telangiectatic-like appearance that is considered pathognomonic for radiation retinopathy [ 111. Clinical features of radiation retinopathy include: intraretinal hemorrhages, hard exudates, cotton wool spots, microaneurysms, telangiectatic vessels, and sheathed retinal vessels (Table 1) [2,5,10]. Eyes exposed to external beam radiation tend to demonstrate more hemorrhages and cotton wool spots, while the local radiation therapy eyes exhibit more exudative changes [5]. The extensive exudative changes seen in local therapy are thought, in part, to be caused by vascular leakage of the intraocular neoplasm [5]. Retinal capillary non-perfusion may vary from minimal to widespread [12]. Neovascularization of the retina or the disc may develop as a sequelae of extensive capillary nonperfusion [5]. Neovascularization of the iris and angle can also ensue. Visual impairment resulting from radiation retinopathy ranges from minimal, to total loss of sight. Decreased vision associated with radiation retinopathy can be attributed to macular nonperfusion, macular edema or exudation, vitreous hemorrhage, neovascular glaucoma, or radiation optic neuropathy [13]. Visual loss related to macular non-perfusion is irreversible, but grid laser photocoagulation may be used to treat macular edema. Panretinal laser photocoagulation is administered for retinal, disc, or iris neovascularization in an attempt to prevent vitreous hemorrhage, tractional retinal detachment, and/or neovascular glaucoma [ 131.
Table 1 Differential
diagnosis of radiation retinopathy
Diabetic retinopathy Hypertensive retinopathy HIV retinopathy Blood dyscrasias Ocular ischemic syndrome
Eye and Vision
Care 8 (1996)
119-122
2. Case report
A 50-year-old Caucasian male presented to the Eye Clinic with a chief complaint of decreased vision in both eyes. The patient had been diagnosed with multiple myeloma for 3 years. The patient’s status was 21 months post autologous bone marrow transplant for IgG Kappa stage III multiple myeloma. In preparation for the transplant, the patient underwent total body irradiation (TBI) of 150 cGy, twice daily for 3 days, totalling 900 cGy. Concurrent with the radiation therapy, chemotherapy was administered consisting of 3.5 mg/kg busulfan daily for 4 days, and 60 mg/kg cyclophosphamide for 2 days. The year preceding the transplant the patient was on a chemotherapeutic regimen. An 18-month remissive state followed his transplant, chemotherapy, and radiation therapy. Unfortunately, the multiple myeloma recurred, again requiring treatment. Current treatment consists of a chemotherapy combination of melphalan 10 mg/prednisone 100 mg daily for 4 days of every month. Recent testing indicates remission, thus treatment may soon be discontinued. Ocular examination revealed best corrected visual acuities (BVA’s) of 20/20-l OD and 20/20 OS with subtle posterior subcapsular cataract (PSC) changes in both eyes. Pupils, intraocular pressures, confrontation fields, extraocular muscles, and all anterior segment findings were normal. Dilated fundus examination revealed cotton wool spots, microaneurysms, and exudates within, and immediately outside, the arcades of both eyes. Over the next five months, BVA’s decreased to 20/25 OD, 20/40 OS, presumably due to progression of the PSC OS more than OD. No other changes in ocular health were noted. The retinal findings in both eyes remained stable and unrelated to the vision loss. 3. Discussion Multiple myeloma is a plasma cell dyscrasia [14] that stems from bone marrow precursor cells [15]. These bone marrow cells initiate malignant proliferation of plasma cells which are specific for production of particular immunoglobulins. Plasma cell tumors most often produce IgG, but may produce IgA, IgD, or IgE. Recommended therapy for multiple myeloma includes combination chemotherapy and radiation therapy resulting in a decrease of myeloma protein production in roughly 75-80% of cases. With treatment, the average post-diagnosis survival time is approximately 2-3 years [15].
M.J. Horn,
SD. Ayers
/Clinical
Eye and Vision
Retinopathy can be caused by multiple myeloma exclusive of radiation therapy. Patients with retinopathy associated with multiple myeloma typically exhibit decreased hemoglobin concentration and platelet counts. A small percentage of patients with multiple myeloma have been noted to have fundus changes consisting of Roth’s spots, flame-shaped hemorrhages, and/or nerve fiber layer infarcts due to the anemia and thrombocytopenia caused by the disease. Less commonly, neovascularization, venous occlusions, and vitreous hemorrhages have been reported in patients with multiple myeloma and associated serum hyperviscosity. These fundus changes are reported to resolve in half of the patients who are treated [15]. In assessing the fundus findings in our patient, the differential diagnosis included diabetes mellitus, hypertension, the human immunodeficiency virus (HIV), pharmacologically induced anemia, ocular manifestations of multiple myeloma, and radiation retinopathy (Table 2). Blood glucose levels, blood pressure assessments, complete blood counts, and an HIV ELISA test were all negative, thus eliminating diabetes, hypertension, pharmacologically-induced anemia, and HIV from the differential. The patient has undergone systemic treatment for approximately 3 years and has normal complete blood counts, indicating that the retinopathy present is unlikely secondary to multiple myeloma. The patient received radiation doses considered to be within safe limits by current radiation therapy guidelines [16], thus ocular protection was not deemed necessary. In addition to his radiation therapy, the patient was also treated with chemotherapy. Patients who are treated with combination chemotherapy and radiation are much more likely to develop retinopathy [5,16]. Radiation therapy and chemotherapy do not have to be administered concomitantly in order to cause this effect [3]. The patient was treated before, during, and after radiation therapy with a variety of chemotherapeutic agents, therefore radiation retinopathy cannot be excluded from the differential diagnosis. The patient was not diabetic, but there is a known synergism between diabetes and radiation retinopaTable 2 Retinal-vascular findings of radiation retinopathy Intraretinal hemorrhages Hard exudates Cotton wool spots Microaneurysms Telangiectatic vessels Sheathed retinal vessels Capillary non-perfusion Neovascularization of retina and/or Diffuse atrophy of RPE
Care 8 (I 996) 119-122
121
thy. Diabetes and radiation appear to affect the retinal capillaries in a similar way [4]. This may help explain the exacerbation of radiation retinopathy in patients with diabetes. We assume that chemotherapeutic agents also have an adverse affect on capillaries, and this might help to explain the increase in radiation retinopathy observed with radiation and chemotherapy in combination. Fortunately, the patient’s retinopathy does not appear to have had a deleterious affect on his vision. The patient’s vision loss in this case is likely related to development of posterior subcapsular cataracts in both eyes. The accelerated cataract development is assumed to be secondary to the prednisone use [17], or to the radiation exposure [18,19,20]. 4. Summary The potential for radiation retinopathy should be considered in the differential diagnosis of retinalvascular anomalies (Table 2). Radiation retinopathy has been reported in association with radiation treatment for such conditions as: ocular neoplasm, thyroid disease, tumors of the central nervous system, tumors of the paranasal sinuses [lo], and tumors of the face and lids [13]. A thorough case history may help identify patients with prior radiation treatments that have the potential to cause ocular manifestations. Determining the dose, number and size of radiation fractions, and the total time of radiation treatment is helpful in assessing a patient’s risk for developing retinopathy. Other risk factors should also be evaluated in patients who have been treated with radiation. Chemotherapy administered in association with radiation increases the chances of retinopathy, as does diabetes. Additionally, it is important to determine if the eyes were shielded during radiation therapy. Shielding the eye during radiation therapy may help prevent damage to the eye. A full ocular health examination is important in a post radiation patient. Additional diagnostic testing may also be necessary, such as fluorescein angiography to diagnose macular non-perfusion. Finally, patients should be educated regarding the possible development of retinopathy associated with their disease and/or treatment and the need for appropriate follow-up. References [t]
ONH
Stallard HB. Glioma retinae treated by radon seeds. Br J Med 1936;962-964. [2] Lopez PF, Stemberg P, Dabbs CK, Vogler WR, Cracker I, Alin NS. Bone marrow transplant retinopathy. Am J Ophthalmol 1991;112:635-646..
122 [31 [41
151
b1 [71
Bl [91
DO1
[ill
M.J. Horn,
SD. Ayers
/Clinical
Chacko DC. Considerations in the diagnosis of radiation injury. J Am Med Assoc 1981;245:1255-1258. Viebahn M, Barricks ME, Oserioh MD. Synergism between diabetic and radiation retinopathy: case report and review. Br J Ophthalmol 1991;75:629-632. Brown GC, Shields JA, Sanbom G, Augsburger JJ, Savino PJ, Schatz NJ. Radiation retinopathy. Ophthalmology 1982; 89:1494-1501. Harris JR, Levene MB. Visual complications following irradiation for pituitary adenomas and craniopharyngiomas. Radiology 1976;120:167-171. Aristizabal S, Caldwell WL, Avila J. The relationship of the time dose fractionation factors to the complications in the treatment of pituitary tumors by irradiation. Int J Radiat Oncol Biol Phys 1977;2:6667-673. Quinn AG, Clemett RS. Retinopathy after low-dose retinal irradiation. Aust N Z J Ophthalmol 1993;21(3):193-197. Brown GC. Radiation retinopathy. In: Duane’s Clinical Ophthalmology. Philadelphia, J.B. Lippincott, 1991. Nakissa N, Rubin P, Strohl R, Keys H. Ocular and orbital complications following radiation therapy of paranasai sinus and review of literature. Cancer malignancies 1983;51:980-986. Archer DB, Amoaku WMK, Gardiner TA. Radiation retinopathy clinical, histopathological, ultrastructural and experimental correlations. Eye 1991;5:239-251.
Eye and Vision
Care 8 (1996)
119-122
Amoaku WMK, Archer DB. Fluorescein angiographic features, natural course and treatment of radiation retinopathy. Eye 1990;4:657-667. 1131 Schachat AP. Radiation retinopathy. In: Retina: Vol.11. St. Louis, C.V. Mosby Co., 1989. Knapp AJ, Gartner S, Henkind P. Multiple myeloma and its D41 ocular manifestations. Ophthalmology 1987;31:343-351. 1151 Lukes RJ, Collins RD. Tumors of the hematopoetic system. Bethesda, MD, Armed Forces Institute of Pathology, 1992130-137. Ml Gordon KB, Char DH, Sager-man RH. Late effects of radiation on the eye and ocular adnexa. Int J Radiat Oncol Biol Phys 119;31:1123-1139. 1171 Shalka HW, Prchal JT. Effect of corticosteroids on cataract formation. Arch Ophthalmol 1980;98:1773-1777. 1181 Pitts DG, Kleinstein RN. Environmental vision: interactions of the eye, vision, and the environment. Boston, Butterworth Heinemann, 204-206. Hayes BP, Fisher RF. Influence of a prolonged period of D91 low-dosage X-rays on the optic and ultrastructural appearances of cataract of the human lens. Br J Ophthalmol 1979;63:457-464.
1201 Bray LC, Carey PJ, Proctor SJ, Evans RGB, Hamilton PJ. Ocular complications of bone marrow transplantation. Ophthalmol 1991;75:611-614.
Br J