Abstract

aclinical evaluation of radiation therapy of lesions of the eye requires close co-operation between the ophthalmologist and the radiologist. The ophthalmologist in general is not qualified, without special training, to carry out radiation treatment, and the radiologist is usually not qualified to employ such therapy without a thorough knowledge of the pathogenesis of the lesion treated. This study represents a co-ordinated effort between the Departments of Radiology and Ophthalmology at Western Reserve University. Prior to 1940, gamma rays from radium and grenz rays were used in radiation therapy for various ophthalmologic conditions. In that year, Burnam and Neill (1) reported on the use of beta rays originating from radon gas, the daughter isotope of radium, contained in a glass bulb enclosed within a brass cylinder. This type of applicator was in general use until artificially produced radioactive isotopes became available. In 1950 two of the present authors (C. I T. and H. L. F.) reported on the use of a Sr90 beta-ray applicator in the treatment of ophthalmologic diseases (2, 3). This applicator had the advantage of being a pure beta particle emitter and, because of the long half-life of Sr90, did not require frequent replenishing. Reports are now available concerning the physical characteristics of the applicator, the biological and therapeutic response to the radiation, and the recommended dosage schedules for treating certain ophthalmologic conditions (4). During the last few years, much has been written concerning the complications observed following beta irradiation of the eve (4. 6. 8. 9). Manv of these changes are the natural sequelae of large doses. They include scleral atrophy, conjunctival scarring, and telangiectasia. The one change that has not been completely evaluated clinically, although it has received widespread attention experimentally, is that which occurs in the lens. Any damage to that structure would appear to be very significant, since it may be associated with impairment of vision. A well established pattern is known to occur, and certain pathological changes take place in a lens exposed to a sufficient amount of radiation (5–8). As a rule, these changes are stationary. Rarely, but especially after high doses of radiation, complete opacity has been observed. The onset of cataract formation ranges from two to ten years after irradiation, depending upon the total dose delivered. Several reports place the maximum as long as fifteen years following exposure to ionizing radiation (5, 6, 9). In general, 500 r is considered potentially dangerous to the human lens (5), while experimental investigations by Leinfelder and Dickerson (15) would indicate that 5,000 r produces a massive insult. Von Sallmann et al. have indicated that direct or indirect injury to cell nuclei by irradiation is dose dependent (8).

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