Delayed Effects of Ionizing Radiation

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Abstract
Practically all the known biologic changes produced by ionizing radiation are in a strict sense delayed effects, since they develop only after a significant latent period. It is customary, however, to limit the term “delayed effects” to those injuries that first become apparent several months or years after exposure. At times no sharp dividing line separates the early from the delayed reactions, but as a rule the two are easily distinguished. Tissues in which delayed effects are destined to appear seldom show a steady progression of injury from the early to the late reaction. Characteristically, the acute response subsides and the tissues resume a fairly normal appearance or at least reach a stable state of relative ischemia. At any time thereafter the late lesions may develop. Most delayed radiation injuries are the consequence of accidental or misguided overexposure. They may develop following large therapeutic doses given in single or multiple exposures or as the cumulative effect of small continuous or intermittent doses absorbed accidentally over the course of years. All types of ionizing radiation, whether delivered from internal or external sources, are effective provided the doses are sufficient. No tissue of the body is immune, but in practice the majority of the late lesions are found to fall into a limited number of well recognized types. Radiation injuries may be separated into two major categories, according to whether they are local or general in nature. Localized lesions usually result from local irradiation but some local lesions, such as cataract, may also follow whole-body exposure. In like fashion, generalized effects are seen most often when either a large area or the entire body has been ex- posed, though heavy local treatment at times produces systemic effects. No detailed description of the various delayed lesions will be attempted, but a few of the commoner types deserve brief mention. Late radiation ulcers usually result from localized radiation therapy. They occur most often in the skin but are seen also in the rectum and bladder and occasionally elsewhere. Even though the dose has been of such a size that late lesions will ultimately develop, the early acute reaction usually heals, leaving a poorly vascularized tissue which is often the seat of telangiectases, chronic edema, and fibrosis. Ulceration begins after an indeterminate latent period of months or years and extends progressively to produce a sharply punched-out ulcer crater with a brawny, indurated, ischemic base. Once the ulcer has developed, it heals poorly if at all, and even if it heals is prone to recur. Ischemia appears to be a major underlying factor in the pathogenesis of ulcerating lesions, although the onset is often precipitated by some secondary injury. Chronic radiation dermatitis, resembling in many respects spontaneous senile degeneration of the skin, may persist for many years without ulceration.

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