Radiation burn

A radiation burn is a damage to the skin or other biological tissue and organs as an effect of radiation. The radiation types of greatest concern are thermal radiation, radio frequency energy, ultraviolet light and ionizing radiation.
The most common type of radiation burn is a sunburn caused by UV radiation. High exposure to X-rays during diagnostic medical imaging or radiotherapy can also result in radiation burns. As the ionizing radiation interacts with cells within the body—damaging them—the body responds to this damage, typically resulting in erythema—that is, redness around the damaged area. Radiation burns are often discussed in the same context as radiation-induced cancer due to the ability of ionizing radiation to interact with and damage DNA, occasionally inducing a cell to become cancerous. Cavity magnetrons can be improperly used to create surface and internal burning. Depending on the photon energy, gamma radiation can cause deep gamma burns, with ⁶⁰Co internal burns common. Beta burns tend to be shallow as beta particles are not able to penetrate deeply into a body; these burns can be similar to sunburn. Alpha particles can cause internal alpha burns if inhaled, with external damage being limited to minor erythema.
Radiation burns can also occur with high power radio transmitters at any frequency where the body absorbs radio frequency energy and converts it to heat. The U.S. Federal Communications Commission considers 50 watts to be the lowest power above which radio stations must evaluate emission safety. Frequencies considered especially dangerous occur where the human body can become resonant, at 35 MHz, 70 MHz, 80-100 MHz, 400 MHz, and 1 GHz. Exposure to microwaves of too high intensity can cause microwave burns.

Types

Radiation dermatitis is a skin disease associated with prolonged exposure to ionizing radiation. Radiation dermatitis occurs to some degree in most patients receiving radiation therapy, with or without chemotherapy.
There are three specific types of radiodermatitis: acute radiodermatitis, chronic radiodermatitis, and eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy. Radiation therapy can also cause radiation cancer.
With interventional fluoroscopy, because of the high skin doses that can be generated in the course of the intervention, some procedures have resulted in early and/or late skin reactions, including necrosis in some cases.
Radiation dermatitis, in the form of intense erythema and vesiculation of the skin, may be observed in radiation ports.
As many as 95% of patients treated with radiation therapy for cancer will experience a skin reaction. Some reactions are immediate, while others may be later.

Acute

Acute radiodermatitis occurs when an "erythema dose" of ionizing radiation is given to the skin, after which visible erythema appears up to 24 hours after. Radiation dermatitis generally manifests within a few weeks after the start of radiotherapy. Acute radiodermatitis, while presenting as red patches, may sometimes also present with desquamation or blistering. Erythema may occur at a dose of 2 Gy radiation or greater.

Chronic

Chronic radiodermatitis occurs with chronic exposure to "sub-erythema" doses of ionizing radiation over a prolonged period, producing varying degrees of damage to the skin and its underlying parts after a variable latent period of several months to several decades. In the past this type of radiation reaction occurred most frequently in radiologists and radiographers who were constantly exposed to ionizing radiation, especially before the use of X-ray filters. Chronic radiodermatitis, squamous and
basal cell carcinomas may develop months to years after radiation exposure. Chronic radiodermatitis presents as atrophic indurated plaques, often whitish or yellowish, with telangiectasia, sometimes with hyperkeratosis.

Other

Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy is a skin condition that occurs most often in women receiving cobalt radiotherapy for internal cancer.
Radiation-induced erythema multiforme may occur when phenytoin is given prophylactically to neurosurgical patients who are receiving whole-brain therapy and systemic steroids.

Delayed effects

Radiation acne is a cutaneous condition characterized by comedo-like papules occurring at sites of previous exposure to therapeutic ionizing radiation, skin lesions that begin to appear as the acute phase of radiation dermatitis begins to resolve.
Radiation recall reactions occur months to years after radiation treatment, a reaction that follows recent administration of a chemotherapeutic agent and occurs with the prior radiation port, characterized by features of radiation dermatitis. Restated, radiation recall dermatitis is an inflammatory skin reaction that occurs in a previously irradiated body part following drug administration. There does not appear to be a minimum dose, nor an established radiotherapy dose relationship.

Alpha burns

"Alpha burns" are caused by alpha particles, which can cause extensive tissue damage if emitted within the body by inhaled or ingested sources. Due to the keratin in the epidermal layer of the skin, external alpha burns are limited to only mild reddening of the outermost layer of skin.

Beta burns

"Beta burns"—caused by beta particles—are shallow surface burns, usually of skin and less often of lungs or gastrointestinal tract, caused by beta particles, typically from hot particles or dissolved radionuclides that came to direct contact with or close proximity to the body. They can appear similar to sunburn. Unlike gamma rays, beta emissions are stopped much more effectively by materials and therefore deposit all their energy in only a shallow layer of tissue, causing more intense but more localized damage. On cellular level, the changes in skin are similar to radiodermatitis.
The dose is influenced by relatively low penetration of beta emissions through materials. The cornified keratine layer of epidermis has enough stopping power to absorb beta radiation with energies lower than 70 keV. Further protection is provided by clothing, especially shoes. The dose is further reduced by limited retention of radioactive particles on skin; a 1 millimeter particle is typically released in 2 hours, while a 50 micrometer particle usually does not adhere for more than 7 hours. Beta emissions are also severely attenuated by air; their range generally does not exceed and intensity rapidly diminishes with distance.
The eye lens seems to be the most sensitive organ to beta radiation, even in doses far below maximum permissible dose. Safety goggles are recommended to attenuate strong beta.
Careful washing of exposed body surface, removing the radioactive particles, may provide significant dose reduction. Exchanging or at least brushing off clothes also provides a degree of protection.
If the exposure to beta radiation is intense, the beta burns may first manifest in 24–48 hours by itching and/or burning sensation that last for one or two days, sometimes accompanied by hyperaemia. After 1–3 weeks burn symptoms appear; erythema, increased skin pigmentation, followed by epilation and skin lesions. Erythema occurs after 5–15 Gy, dry desquamation after 17 Gy, and bullous epidermitis after 72 Gy. Chronic radiation keratosis may develop after higher doses. Primary erythema lasting more than 72 hours is an indication of injury severe enough to cause chronic radiation dermatitis. Edema of dermal papillae, if present within 48 hours since the exposition, is followed by transepidermal necrosis. After higher doses, the malpighian layer cells die within 24 hours; lower doses may take 10–14 days to show dead cells. Inhalation of beta radioactive isotopes may cause beta burns of lungs and nasopharyngeal region, ingestion may lead to burns of gastrointestinal tract; the latter being a risk especially for grazing animals.

In first degree beta burns the damage is largely limited to epidermis. Dry or wet desquamation occurs; dry scabs are formed, then heal rapidly, leaving a depigmented area surrounded with irregular area of increased pigmentation. The skin pigmentation returns to normal within several weeks.
Second degree beta burns lead to formation of blisters.
Third and fourth degree beta burns result in deeper, wet ulcerated lesions, which heal with routine medical care after covering themselves with dry scab. In case of heavy tissue damage, ulcerated necrotic dermatitis may occur. Pigmentation may return to normal within several months after wound healing.

Lost hair begins regrowing in nine weeks and is completely restored in about half a year.
The acute dose-dependent effects of beta radiation on skin are as follows:

0–6 Gy	no acute effect
6–20 Gy	moderate early erythema
20–40 Gy	early erythema in 24 hours, skin breakdown in 2 weeks
40–100 Gy	severe erythema in less than 24 hours
100–150 Gy	severe erythema in less than 4 hours, skin breakdown in 1–2 weeks
150–1000 Gy	blistering immediate or up to 1 day

According to other source:

2–6 Gy	transient erythema 2–24 h
3–5 Gy	dry desquamation in 3–6 weeks
3–4 Gy	temporary epilation in 3 weeks
10–15 Gy	erythema 18–20 days
15–20 Gy	moist desquamation
25 Gy	ulceration with slow healing
30–50 Gy	blistering, necrosis in 3 weeks
100 Gy	blistering, necrosis in 1–3 weeks

As shown, the dose thresholds for symptoms vary by source and even individually. In practice, determining the exact dose tends to be difficult.
Similar effects apply to animals, with fur acting as additional factor for both increased particle retention and partial skin shielding. Unshorn thickly wooled sheep are well protected; while the epilation threshold for sheared sheep is between 23 and 47 Gy and the threshold for normally wooled face is 47–93 Gy, for thickly wooled sheep it is 93–140 Gy. To produce skin lesions comparable with contagious pustular dermatitis, the estimated dose is between 465 and 1395 Gy.