Radiation dermatitis

Radiation dermatitis develops as a result of exposure to ionizing radiation. The nature of skin changes depends on the intensity of the radiation exposure. They can be acute, developing after a short latent period, and chronic, occurring after a few months or even years after irradiation. Acute radiation damage to the skin can be in the form of erythematous, bullous or necrotic reactions, after the disappearance of which can remain atrophic, cicatricial changes, telangiectasias, and long-lasting non-healing ulcers. Chronic radiation damage usually occurs when exposure to small doses of ionizing radiation. Characterized by poorly pronounced inflammation, poikilodermia, a tendency to hyperplastic processes in the epidermis, especially with ulcerative lesions. Against the background of such changes, skin cancer often occurs.

[1], [2], [3], [4], [5]

Pathomorphology of radiation dermatitis

A typical microscopic picture with acute radiation dermatitis is characterized by a strong edema of the upper parts of the dermis, as a result of which the epidermis is flattened, epidermal outgrowths are absent. In the dermis - homogenization of collagen and swelling of the capillaries, accompanied by narrowing and closing of their lumens; occasionally infiltration of neutrophilic granulocytes and lymphocytes around the sweat glands occurs. The sebaceous glands are not changed. Sometimes there is a vacuolization of the cells of the baal layer of the epidermis, the appearance of large atypical many nuclear cells resembling those of Korn's disease.

Around the focus of the lesion, thinning of the epidermis, an increase in the amount of pigment in the basal cells and melanocytes, as well as melanophages of the dermis are noted. Around the dilated vessels, the number of fibroblastic elements increases. In the future, hyperkeratosis, atrophy of the epidermis and hair follicles, vacuolation of the basal layer cells develop.

In chronic radiation dermatitis, the histological picture depends on the degree of damage. Almost always find fibrotic changes in the walls of the vessels, especially the deep sections of the dermis, with more or less narrowing of their lumen, fibrosis and homogenization, and sometimes hyalinization of connective tissue. In cases clinically accompanied by telangiectasia, there are significant changes in the vessels in the upper parts of the dermis. Changes in the epidermis are different, from atrophy to acanthosis and hyperkeratosis. In the germ layer of the epidermis, there are lesions of cells resembling those of Bowen's disease: dyskeratosis and atypia, uneven epidermal outgrowths in the dermis. As a result of obliteration of blood vessels ulcers can form, along the edges of which pseudoepithelioma epidermal hyperplasia is often found. In the dermis, there is a proliferation of connective tissue with a large number of cellular elements and melanin both inside the melanophages and outside them. Many collagen fibers are fragmented, disposed unoriented, and elastic fibers also with fragmentation phenomena, but to a lesser extent. Skin attachments are atrophied until they disappear completely. These changes can lead to the development of squamous cell carcinoma of the skin.