Radiation injury

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Radiation poisoning, also called radiation sickness, is a form of damage to organ tissue due to excessive exposure to ionizing radiation. The term is generally used to refer to acute problems caused by a large dosage of radiation in a short period. Many of the symptoms of radiation poisoning occur as ionizing radiation interferes with cell division. This interference allows for treatment of cancer cells; such cells are among the fastest-dividing in the body, and may be destroyed by a radiation dose that adjacent normal cells are likely to survive.

The clinical name for “radiation sickness” is acute radiation syndrome as described by the CDC[2][3][4][5]. A chronic radiation syndrome does exist but is very uncommon; this has been observed among workers in early radium source production sites and in the early days of the Soviet nuclear program. A short exposure can result in acute radiation syndrome; chronic radiation syndrome requires a prolonged high level of exposure.

The rad is a unit of absorbed radiation dose defined in terms of the energy actually deposited in the tissue. One rad is an absorbed dose of 0.01 joules of energy per kilogram of tissue. The more recent SI unit is the gray (Gy), which is defined as 1 joule of deposited energy per kilogram of tissue. Thus one gray is equal to 100 rad.

To accurately assess the risk of radiation, the absorbed dose energy in rad is multiplied by the relative biological effectiveness (RBE) of the radiation to get the biological dose equivalent in rems. Rem stands for “Röntgen equivalent in man (sic).” In SI units, the absorbed dose energy in grays is multiplied by the same RBE to get a biological dose equivalent in sieverts (Sv). The sievert is equal to 100 rem.

The RBE is a “quality factor,” often denoted by the letter Q, which assesses the damage to tissue caused by a particular type and energy of radiation. For alpha particles Q may be as high as 20, so that one rad of alpha radiation is equivalent to 20 rem. The Q of neutron radiation depends on their energy. However, for beta particles, x-rays, and gamma rays, Q is taken as one, so that the rad and rem are equivalent for those radiation sources, as are the gray and sievert. See the sievert article for a more complete list of Q values.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Injury to the skin and underlying tissues from acute exposure to a large external dose of radiation is referred to as cutaneous radiation injury (CRI). Acute radiation syndrome (ARS) 1 will usually be accompanied by some skin damage; however, CRI can occur without symptoms of ARS. This is especially true with acute exposures to beta radiation or low-energy x-rays, because beta radiation and low-energy x-rays are less penetrating and less likely to damage internal organs than gamma radiation is. CRI can occur with radiation doses as low as 2 Gray (Gy) or 200 rads 2 and the severity of CRI symptoms will increase with increasing doses. Most cases of CRI have occurred when people inadvertently came in contact with unsecured radiation sources from food irradiators, radiotherapy equipment, or well depth gauges. In addition, cases of CRI have occurred in people who were overexposed to x-radiation from fluoroscopy units.

Early signs and symptoms of CRI are itching, tingling, or a transient erythema or edema without a history of exposure to heat or caustic chemicals. Exposure to radiation can damage the basal cell layer of the skin and result in inflammation, erythema, and dry or moist desquamation. In addition, radiation damage to hair follicles can cause epilation. Transient and inconsistent erythema (associated with itching) can occur within a few hours of exposure and be followed by a latent, symptom-free phase lasting from a few days to several weeks. After the latent phase, intense reddening, blistering, and ulceration of the irradiated site are visible. Depending on the radiation dose, a third and even fourth wave of erythema are possible over the ensuing months or possibly years.

In most cases, healing occurs by regenerative means; however, large radiation doses to the skin can cause permanent hair loss, damaged sebaceous and sweat glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or necrosis of the exposed tissue.

With CRI, it is important to keep the following things in mind:

• The visible skin effects depend on the magnitude of the dose as well as the depth of penetration of the radiation.

• Unlike the skin lesions caused by chemical or thermal damage, the lesions caused by radiation exposures do not appear for hours to days following exposure, and burns and other skin effects tend to appear in cycles.

• The key treatment issues with CRI are infection and pain management.

CRI will progress over time in stages and can be categorized by grade, with characteristics of the stages varying by grade of injury, as shown in Table 1. Appendix A gives a detailed description of the various skin responses to radiation, and Appendix B provides color photographs of examples of some of these responses.

Prodromal stage (within hours of exposure)—This stage is characterized by early erythema (first wave of erythema), heat sensations, and itching that define the exposure area. The duration of this stage is from 1 to 2 days.

Latent stage (1–2 days postexposure)—No injury is evident. Depending on the body part, the larger the dose, the shorter this period will last. The skin of the face, chest, and neck will have a shorter latent stage than will the skin of the palms of the hands or the soles of the feet.

Manifest illness stage (days to weeks postexposure)—The basal layer is repopulated through proliferation of surviving clonogenic cells. This stage begins with main erythema (second wave), a sense of heat, and slight edema, which are often accompanied by increased pigmentation. The symptoms that follow vary from dry desquamation or ulceration to necrosis, depending on the severity of the CRI (see Table 1).

Third wave of erythema (10–16 weeks postexposure, especially after beta exposure)—The exposed person experiences late erythema, injury to blood vessels, edema, and increasing pain. A distinct bluish color of the skin can be observed. Epilation may subside, but new ulcers, dermal necrosis, and dermal atrophy (and thinning of the dermis layer) are possible.

Late effects (months to years postexposure; threshold dose ~10 Gy or 1000 rads)—Symptoms can vary from slight dermal atrophy (or thinning of dermis layer) to constant ulcer recurrence, dermal necrosis, and deformity. Possible effects include occlusion of small blood vessels with subsequent disturbances in the blood supply (telangiectasia); destruction of the lymphatic network; regional lymphostasis; and increasing invasive fibrosis, keratosis, vasculitis, and subcutaneous sclerosis of the connective tissue. Pigmentary changes and pain are often present. Skin cancer is possible in subsequent years.

Recovery (months to years)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Acute Radiation Syndrome (ARS) (sometimes known as radiation toxicity or radiation sickness) is an acute illness caused by irradiation of the entire body (or most of the body) by a high dose of penetrating radiation in a very short period of time (usually a matter of minutes). The major cause of this syndrome is depletion of immature parenchymal stem cells in specific tissues. Examples of people who suffered from ARS are the survivors of the Hiroshima and Nagasaki atomic bombs, the firefighters that first responded after the Chernobyl Nuclear Power Plant event in 1986, and some unintentional exposures to sterilization irradiators.^[1]

The required conditions for Acute Radiation Syndrome (ARS) are:

• The radiation dose must be large (i.e., greater than 0.7 Gray (Gy)1, 2 or 70 rads).

• Mild symptoms may be observed with doses as low as 0.3 Gy or 30 rads.

• The dose usually must be external ( i.e., the source of radiation is outside of the patient’s body).

• Radioactive materials deposited inside the body have produced some ARS effects only in extremely rare cases.

• The radiation must be penetrating (i.e., able to reach the internal organs).

• High energy X-rays, gamma rays, and neutrons are penetrating radiations.

• The entire body (or a significant portion of it) must have received the dose3.

• Most radiation injuries are local, frequently involving the hands, and these local injuries seldom cause classical signs of ARS.

• The dose must have been delivered in a short time (usually a matter of minutes).

• Fractionated doses are often used in radiation therapy. These are large total doses delivered in small daily amounts over a period of time. Fractionated doses are less effective at inducing ARS than a single dose of the same magnitude.

The three classic Acute Radiation Syndromes are;

• Bone marrow syndrome (sometimes referred to as hematopoietic syndrome) the full syndrome will usually occur with a dose between 0.7 and 10 Gy (70 – 1000 rads) though mild symptoms may occur as low as 0.3 Gy or 30 rads4.

• The survival rate of patients with this syndrome decreases with increasing dose. The primary cause of death is the destruction of the bone marrow, resulting in infection and hemorrhage.

• Gastrointestinal (GI) syndrome: the full syndrome will usually occur with a dose greater than approximately 10 Gy (1000 rads) although some symptoms may occur as low as 6 Gy or 600 rads.

• Survival is extremely unlikely with this syndrome. Destructive and irreparable changes in the GI tract and bone marrow usually cause infection, dehydration, and electrolyte imbalance. Death usually occurs within 2 weeks.

• Cardiovascular (CV)/ Central Nervous System (CNS) syndrome: the full syndrome will usually occur with a dose greater than approximately 50 Gy (5000 rads) although some symptoms may occur as low as 20 Gy or 2000 rads.

• Death occurs within 3 days. Death likely is due to collapse of the circulatory system as well as increased pressure in the confining cranial vault as the result of increased fluid content caused by edema, vasculitis, and meningitis.

The four stages of ARS are;

• Prodromal stage (N-V-D stage): The classic symptoms for this stage are nausea, vomiting, as well as anorexia and possibly diarrhea (depending on dose), which occur from minutes to days following exposure. The symptoms may last (episodically) for minutes up to several days.
• Latent stage: In this stage, the patient looks and feels generally healthy for a few hours or even up to a few weeks.
• Manifest illness stage: In this stage the symptoms depend on the specific syndrome (see Table 1) and last from hours up to several months.
• Recovery or death: Most patients who do not recover will die within several months of exposure. The recovery process lasts from several weeks up to two years.

The concept of cutaneous radiation syndrome (CRS) was introduced in recent years to describe the complex pathological syndrome that results from acute radiation exposure to the skin.

ARS usually will be accompanied by some skin damage. It is also possible to receive a damaging dose to the skin without symptoms of ARS, especially with acute exposures to beta radiation or X-rays. Sometimes this occurs when radioactive materials contaminate a patient’s skin or clothes.

When the basal cell layer of the skin is damaged by radiation, inflammation, erythema, and dry or moist desquamation can occur. Also, hair follicles may be damaged, causing epilation. Within a few hours after irradiation, a transient and inconsistent erythema (associated with itching) can occur. Then, a latent phase may occur and last from a few days up to several weeks, when intense reddening, blistering, and ulceration of the irradiated site are visible. In most cases, healing occurs by regenerative means; however, very large skin doses can cause permanent hair loss, damaged sebaceous and sweat glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or necrosis of the exposed tissue.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

External exposure is exposure which occurs when the radioactive source (or other radiation source) is outside (and remains outside) the organism which is exposed. Below are a series of three examples of external exposure.

• A person who places a sealed radioactive source in their pocket
• A space traveller who is irradiated by cosmic rays
• A person who is treated for cancer by either teletherapy or brachytherapy. While in brachytherapy the source is inside the person it is still external exposure because the active part of the source never comes into direct contact with the biological tissues of the person.

One of the key points is that external exposure is often relatively easy to estimate, and if the irradiated objects do not become radioactive (except for a case where the radiation is an intense neutron beam which causes activation of the object’). It is possible for an object to be contaminated on the outer surfaces, assuming that no radioactivity enters the object it is still a case of external exposure and it is normally the case that decontamination is easy (wash the surface).

Internal exposure is when the radioactive material enters the organism, and the radioactive atoms become incorporated into the organism. Below are a series of examples of internal exposure.

• The exposure due to Isotopes of potassium-40K (⁴⁰K) present within a normal person.
• The exposure to the ingestion of a soluble radioactive substance, such as Strontium-90 (⁹⁰Sr) in cow’s milk.
• A person who is being treated for cancer by means of an open source radiotherapy method where a radioisotope is used as a drug. A review of this topic was published in 1999.^[1]

Because the radioactive material becomes intimately mixed with the affected object it is often difficult to decontaminate the object or person in a case where internal exposure is occurring. While some very insoluble materials such as fission products within a uranium dioxide matrix might never be able to truly become part of an organism, it is normal to consider such particles in the lungs as a form of internal contamination which results in internal exposure. The reasoning is that the particles have entered via an orifice and can not be removed with ease from what the lay person (non biologist) would regard as within the animal. It is important to note that strictly speaking the contents of the digestive tract and the air within the lungs are outside the body of a mammal.

Nuclear warfare is made more complex by virtue of the fact that a person can be irradiated by at least three processes. The first (the major cause of burns) is not caused by ionizing radiation.

• Thermal burns from infrared heat radiation.
• Beta burns from shallow ionizing radiation (this would be from fallout particles, the largest particles in local fallout would be likely to have very high activities due to the fact that they would be deposited so soon after detonation and it is likely that one such particle upon the skin would be able to cause a localized burn), however these particles are very weakly penetrating and have a short range.
• Gamma burns from highly penetrating radiation, this would be likely to cause deep gamma penetration within the body which would result in uniform whole body irradiation rather than only a surface burn. In cases of whole body gamma irradiation (circa 10 Gy) due to accidents involving medical product irradiators some of the human subjects have developed injuries to their skin between the time of irradiation and death.

In the picture on the right the normal clothing that the woman was wearing would have been unable to attenuate the gamma radiation and it is likely that any such effect was evenly applied to her entire body. Beta burns would be likely all over the body due to contact with fallout, but thermal burns are often on one side of the body as heat radiation does not penetrate the human body. In addition, the pattern on her clothing has been burnt into the skin. This is due to the fact that white fabric reflects more infra-red light than dark fabric. As a result the skin close to dark fabric is burnt more than the skin covered by white clothing.

In addition, there is the risk of internal radiation poisoning by ingestion of fallout particles.

Radiation poisoning can result from accidental exposure to industrial radiation sources. People working with radioactive materials often wear dosimeters or film “badges” to monitor their total exposure to radiation. These devices are more useful than Geiger counters for determining biological effects, as they measure cumulative exposure over time, and are calibrated to change color or otherwise signal the user before exposure reaches unsafe levels. However, film badge types require the film to be developed, as with photographic film, and are used to measure long-term exposure where brief catastrophic exposures are not expected.

Radiation poisoning was a major concern after the Chernobyl reactor accident. It is important to note that in humans the acute effects were largely confined to the accident site. Thirty-one people died as an immediate result.

Of the 100 million curies (4 exabecquerels) of radioactive material, the short lived radioactive isotopes such as ¹³¹I Chernobyl released were initially the most dangerous. Due to their short half-lives of 5 and 8 days they have now decayed, leaving the more long-lived caesium-137 (¹³⁷Cs (with a half-life of 30.07 years) and strontium-90 (⁹⁰Sr (with a half-life of 28.78 years) as main dangers.

Improper handling of radioactive and nuclear materials lead to radiation release and radiation poisoning. The most serious of these, due to improper disposal of a medical device containing a radioactive source (teletherapy), occurred in Goiânia, Brazil in 1987. It is noteworthy that while the majority of accidents involve smaller industrial radioactive sources (typically used for radiography) a large number of the deaths which have occurred have been due to exposure to the larger sources used for medical purposes.

When radioactive compounds enter the human body, the effects are different from those resulting from exposure to an external radiation source. Especially in the case of alpha radiation, which normally does not penetrate the skin, the exposure can be much more damaging after ingestion or inhalation. The radiation exposure is normally expressed as a committed effective dose equivalent (CEDE).

On November 23, 2006, Alexander Litvinenko died due to suspected deliberate poisoning with polonium-210. His is the first case of confirmed death due to such a cause, although it is also known that there have been other cases where radioactive thallium was used. In addition, an incident occurred in 1990 at Point Lepreau Nuclear Generating Station where several employees acquired small doses of radiation due to the contamination of water in the office watercooler with tritium contaminated heavy water.

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Radiation injury should be differentiated from other diseases causing severe headache for example: ^{[1][2][3][4][5][6][7][8][9][10]}

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• Acute epidermal necrosis (time of onset: < 10 days postexposure; threshold dose: ~550 Gy or 55,000 rads)— Interphase death of postmitotic keratinocytes in the upper visible layers of the epidermis (may occur with high-dose, low-energy beta irradiation)

• Acute ulceration (time of onset: < 14 days postexposure; threshold dose: ~20 Gy or 2000 rads)—Early loss of the epidermis— and to a varying degree, deeper dermal tissue—that results from the death of fibroblasts and endothelial cells in interphase

• Dermal atrophy (time of onset: > 26 weeks postexposure; threshold dose: ~10 Gy or 1000 rads)— Thinning of the dermal tissues associated with the contraction of the previously irradiated area

• Dermal necrosis (time of onset > 10 weeks postexposure; threshold dose: ~20 Gy or 2000 rads)— Necrosis of the dermal tissues as a consequence of vascular insufficiency

• Dry desquamation (time of onset: 3–6 weeks postexposure; threshold dose: ~8 Gy or 800 rads)— Atypical keratinization of the skin caused by the reduction in the number of clonogenic cells within the basal layer of the epidermis

• Early transient erythema (time of onset: within hours of exposure; threshold dose: ~2 Gray [Gy] or 200 rads)— Inflammation of the skin caused by activation of a proteolytic enzyme that increases the permeability of the capillaries

• Epilation (time of onset: 14–21 days; threshold dose: ~3 Gy or 300 rads)— Hair loss caused by the depletion of matrix cells in the hair follicles

• Late erythema (time of onset: 8–20 weeks postexposure; threshold dose: ~20 Gy or 2000 rads)— Inflammation of the skin caused by injury of blood vessels. Edema and impaired lymphatic clearance precede a measured reduction in blood flow.

• Invasive fibrosis (time of onset: months to years postexposure; threshold dose: ~20 Gy or 2000 rads)— Method of healing associated with acute ulceration, secondary ulceration, and dermal necrosis that leads to scar tissue formation

• Main erythema (time of onset: days to weeks postexposure; threshold dose: ~3 Gy or 300 rads)— Inflammation of the skin caused by hyperaemia of the basal cells and subsequent epidermal hypoplasia (see photos 1 and 2)

• Moist desquamation (time of onset: 4–6 weeks postexposure; threshold dose: ~15 Gy or 1500 rads)— Loss of the epidermis caused by sterilization of a high proportion of clonogenic cells within the basal layer of the epidermis

• Secondary ulceration (time of onset: > 6 weeks postexposure; threshold dose: ~15 Gy or 1500 rads)— Secondary damage to the dermis as a consequence of dehydration and infection when moist desquamation is severe and protracted because of reproductive sterilization of the vast majority of the clonogenic cells in the irradiated area

• Telangiectasia (time of onset: > 52 weeks postexposure; threshold dose for moderate severity at 5 years: ~40 Gy or 4000 rads)— Atypical dilation of the superficial dermal capillaries.

Radiation sickness is generally associated with acute exposure and has a characteristic set of symptoms that appear in an orderly fashion. The symptoms of radiation sickness become more serious (and the chance of survival decreases) as the dosage of radiation increases. These effects are described as the deterministic effects of radiation.

Longer term exposure to radiation, at doses less than that which produces serious radiation sickness, can induce cancer as cell-cycle genes are mutated. If a cancer is radiation-induced, then the disease, the speed at which the condition advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the sufferer is exposed.

Since tumors grow by abnormally rapid cell division, the ability of radiation to disturb cell division is also used to treat cancer (see radiotherapy), and low levels of ionizing radiation have been claimed to lower one’s risk of cancer (see hormesis).

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