|Carolyn Johns, MSN, RN|
|University of Pennsylvania School of Nursing|
| Last Modified: August 21, 2012
Radiation therapy is a core treatment modality for many types of cancer. Approximately 75% of oncology patients will receive radiation therapy as a component of curative or palliative care (American Society for Radiation Oncology, 2010). Radiotherapy works by delivering a precise dose of radiation to the tumor and damaging the cancer cell’s DNA, thus impairing cell growth and triggering cell death (American Society for Radiation Oncology, 2010). DNA damage may occur both directly, from exposure to irradiation, and indirectly, via water ionization and free radical production (Hymes, Strom, & Fife, 2006). The goal of radiotherapy is to irradiate tumor cells while minimizing damage to normal tissue. However, normal cells in the radiation field may also be damaged by radiation exposure. Typically, normal tissues are capable of self-repair, but repetitive radiation exposure creates an imbalance of tissue damage and repair (Hymes, Strom, & Fife, 2006). The most common example of normal tissue damage as a result of radiotherapy is radiation-induced skin changes, or radiodermatitis. Approximately 95% of radiation oncology patients will experience radiodermatitis and 87% will experience moderate to severe radiodermatitis during or after their therapy (McQuestion, 2006; Fisher et al., 2000). Radiodermatitis may be acute or chronic, and includes localized erythema and edema, skin shedding (desquamation), hair loss (epilation), fibrosis, and necrosis. Radiodermatitis can be painful and embarrassing, and has been associated with decreased quality of life (Fisher et al., 2000). Furthermore, severe radiodermatitis necessitates treatment modifications or delays, which may compromise the efficacy of radiotherapy (Hymes, Strom, & Fife, 2006). Given the scope and severity of radiodermatitis, it is crucial that oncology nurses are familiar with the clinical presentation and evidenced-based interventions for radiodermatitis.
However, an investigative survey by D'haese et al. (2005) found that there is wide discrepancy between nursing interventions for the prevention and management of radiodermatitis. D’haese et al. interviewed radiation oncology nurses in Belgium and found only a small to moderate level of agreement between nurses regarding the prevention and management of radiodermatitis. The greatest variation was between preventative practices. These results suggest that there is confusion among oncology nurses, and likely their patients, regarding the prevention and management of radiodermatitis.
The skin is the largest organ of the body and is composed of two layers, the epidermis and the dermis. The most superficial layer, the epidermis, is made up of a thin layer (< 2 mm) of keratinized squamous cells that serve as a protective barrier against pathogens and prevent water loss from the body (McQuestion, 2006). The dermal layer is slightly thicker (1-3 mm) and contains blood vessels that nourish the skin and assist with thermoregulation (Harper, Franklin, Jenrette, & Aguero, 2004). The dermis also contains nerves that are responsible for sensation, glands that are involved in immune function, and hair follicles (McQuestion, 2006). The skin is continually renewing itself. New skin cells proliferate and mature at the dermal layer and migrate to the epidermis over a period of two to three weeks (Harper et al., 2004).
Radiodermatitis may be acute or chronic and exists on a continuum of erythema, epilation, desquamation, ulceration, or necrosis. Acute skin changes occur within 90 days of initiating therapy as a result of cytokine-mediated inflammation and DNA damage (Hymes, Strom, and Fife, 2006; Muller, Khan, Port, Abend, Molls, Ring, & Meineke, 2006). Erythema and swelling may begin within hours or days of initiating radiation therapy due to the release of cytokines that cause capillary dilation, leukocyte infiltration, and localized swelling (Hymes, Strom, and Fife, 2006; McQuestion, 2006). Dryness and epilation may occur within days to weeks due to damage of sebaceous glands and hair follicles in the dermal layer (McQuestion, 2006). Dry desquamation, characterized by dryness, scaling, and pruritus, typically can occur after the third week or after a cumulative dose of 30 Gy due to destruction of regenerative basal cells (Richardson, Smith, McIntyre, Thomas, & Pilkington, 2005). Dry desquamation typically resolves within one to two weeks of therapy (McQuestion, 2006). Moist desquamation, evidenced by red, exposed dermis and serous oozing, occurs after four to five weeks of therapy or with 45 to 60 Gy cumulative dose as the basal cells are further depleted (Richardson et al., 2005). Acute radiodermatitis usually resolves within three to four weeks after therapy (McQuestion, 2006).
Late effects can occur anywhere from 90 days to years after completing therapy as a result of permanent damage to the dermis (Harper, Franklin, Jenrette, & Aguero, 2004). Late radiation-induced skin changes include atrophy, fibrosis, telangiectasias, and pigmentation changes. Radiation destroys fibroblasts in the dermis, resulting in reabsorption of collagen and tissue atrophy (Harper et al., 2004). However, radiation also stimulates the growth of atypical fibroblasts which produce dense, fibrous tissue (Harper et al., 2004). Radiation-induced fibrosis is characterized by progressive induration, edema, and thickening of the dermis (Harper et al., 2004). Radiation also damages the vasculature of the dermal layer and blood vessels become prominent, dilated, and thin, also known as telangiectasias (Harper et al., 2004). Irradiation exposure may destroy the dermal melanocytes, leading to hypopigmentation, or it may trigger the increased production of melanin in the skin, causing hyperpigmentation (Harper et al., 2004).
Clinical Presentation/Risk Factors
The assessment of radiodermatitis should utilize a validated assessment tool. The Radiation Therapy Oncology Group (RTOG) and the National Cancer Institute (NCI) have established similar assessment tools that classify radiodermatitis by severity. (Appendix 1).
In brief, mild radiodermatitis (RTOG and NCI Grade 1) is characterized by mild, blanchable, erythema or dry desquamation. The onset is typically within days to weeks of initiating therapy and symptoms may fade within a month (McQuestion, 2006). Dry desquamation may be associated with pruritus, epilation, scaling, and possibly changes in pigmentation. Patients with mild radiodermatitis may report that their skin feels tight (McQuestion, 2006). Hair loss occurs in the treatment field and is often temporary, but may become permanent in some patients (McQuestion, 2006).
Moderate radiodermatitis (Grade 2) is often painful and presents as edema and moist desquamation that is localized to the skin folds (Hymes, Strom, & Fife, 2006). Bullae may also be present. It is important to note that wet desquamation indicates that the integrity of the dermis is impaired and thus patients are at increased risk for infection with Staphylococcus aureus (Hymes, Strom, & Fife, 2006). Therefore patients with wet desquamation should be monitored for evidence of infection, such as purulent drainage and fevers, and educated on the need to report any symptoms of infection.
In severe radiodermatitis (Grade 3 and 4), the area of moist desquamation has spread to areas outside of the skin folds. Grade 4 radiodermatitis indicates that ulcers, hemorrhages, and/or tissue necrosis is present. Ulcers may be red with raised edges with a red or black base (McQuestion, 2006). Unfortunately, ulceration is very painful and does not heal well (Gerlach, 2005).
Chronic skin changes may not develop for months or years after radiation therapy. Chronic radiodermatitis results from permanent changes to the dermal layer, resulting in fibrosis, telangiectasias, epilation, and atrophy. The RTOG also has established grading criteria that are specific for chronic radiodermatitis. In summary, grade 1 is characterized by slight atrophy. In grade 2 there are patchy areas of atrophy, telangiectasias, and epilation. Marked atrophy and gross telangiectasias meets RTOG criteria for grade 3. Grade 4 chronic radiodermatitis involves ulceration.
Risk factors for radiodermatitis may be treatment-related or patient-related. Treatment-related risk factors include: type/quality of beam, total dose and fractionation, the location and size of the treatment field, and presence of overlapping fields (Hymes, Strom, & Fife, 2006; Bernier et al., 2008). In general, a patient’s risk for radiodermatitis is proportional to degree of skin exposure to irradiation. Modern radiotherapy techniques, including intensity-modulated radiation therapy (IMRT) and proton therapy, can minimize risk for radiodermatitis by more precisely targeting tumor and thus sparing normal tissue. Consequentially, IMRT has been found to significantly decrease acute radiodermatitis (McDonald, Godette, Butler, Davis, and Johnstone, 2008; Pignol et al., 2008). Dose fractionation delivers a smaller daily radiation dose and has also been found to decrease risk for radiodermatitis (Chan, Teoh, Sanghera, & Hartley, 2009). Specific medications, including some chemotherapy agents, are known to be radio-sensitizers that potentiate the effect of radiation and may increase a patient’s risk for side effects such as radiodermatitis. Concurrent chemoradiotherapy may also increase and prolong radiodermatitis (Giro et al., 2009).
Patient-related risk factors include: obesity and presence of skin folds, poor nutritional status, smoking, concurrent UV exposure, individual radiosensitivity, and comorbid conditions such as ataxia-telangiectasias and autoimmune diseases (Yarbro, Frogge, & Goodman, 2004; Hymes, Strom, & Fife, 2006). Skin folds within the radiation field intensify the dose that is delivered to that specific area thus increasing risk for toxicity. Poor nutritional status and smoking may exacerbate radiodermatitis by impairing wound healing. Autoimmune illnesses, such as scleroderma, systemic lupus erythematosus, and possibly rheumatoid arthritis, are believed to be indicators of increased radiosensitivity (Hymes, Strom, & Fife, 2006). There are also a few rare genetic mutations that may predispose patients to severe radiodermatitis, including mutations in the ataxia telangiectasias (ATM) gene and patched (PTCH) gene (Hymes, Strom, & Fife, 2006).
The patient’s treatment history, specifically the duration of and cumulative dose of radiotherapy, will provide the best clue as to the diagnosis of radiodermatitis. However, there are several other differential diagnoses to consider that include radiation recall, cellulitis, eczema, and secondary malignancy.
Radiation recall is an inflammatory skin reaction that occurs in a previously irradiated area following drug administration. Cytotoxic drugs such as docetaxel, doxorubicin, and paclitaxel have been associated with radiation recall (Chen et al, 2009; Yeo & Johnson, 2000). Radiation recall may present as erythema, ulceration, hemorrhage, or even necrosis and may occur months to years after radiation therapy (Hymes, Strom, & Fife, 2006). Radiation recall generally resolves spontaneously with symptom management and supportive care (Yeo & Johnson, 2000). An accurate history of the patient’s radiation treatment and medications will help to determine whether dermatitis may be due to radiation recall.
Cellulitis is an infection of the dermis or subcutaneous tissues that is characterized by localized redness, swelling, fevers and possibly purulent drainage (Fiebach, Kern, Thomas, & Ziegelstein, 2007). Altered skin integrity secondary to radiodermatitis may predispose a patient to cellulitis (Hill, Bogle, & Duvic, 2004). Other risk factors for cellulitis include weakened immune system, chronic swelling as with lymphedema, and skin conditions such as eczema (Stevens & Eron, 2009). The diagnosis of cellulitis may be confirmed by a culture of the wound drainage or may be treated empirically with antibiotics (Fiebach, Kern, Thomas, & Ziegelstein, 2007). The key difference between radiodermatitis and cellulitis is that patients with cellulitis will present with evidence of infection, such as purulent drainage and fevers.
Eczema, or atopic dermatitis, is a chronic, relapsing, inflammatory skin condition that is diagnosed by clinical presentation of symmetrical, pruritic, dry skin that persists for greater than six months (Saeki et al., 2009). In adults, eczema tends to be worse on the face, chest, and back (Saeki et al., 2009). Chronic eczema may exacerbate radiodermatitis as both conditions are inflammatory in nature (Hymes, Strom, and Fife, 2006). The treatment for eczema is based on symptom severity, but often includes a combination of topical moisturizer and topical corticosteroid (Saeki et al., 2009). Eczema may be distinguished from radiodermatitis by its symmetrical distribution. In contrast, radiodermatitis will only appear in radiation fields.
A secondary skin malignancy, although a rare side effect of radiation, needs to be ruled out (Pierard, Pierard-Franchemont, Paquet, & Quatresoaz, 2009). Furthermore, the incidence of primary skin cancer is high; approximately one in five Americans will develop skin cancer in their lifetime (American Cancer Society, 2008). The presentation of skin cancer varies by type, but may include atypical skin lesions with irregular borders, color variation, and asymmetry (Gordon, 2009). Risk factors for skin cancer include fair skin, history of severe sun burns, personal or family history of skin cancer, history of dysplastic nevi, sun or tanning bed exposure, and a weakened immune system (Gordon, 2009). A skin biopsy is needed to confirm malignancy and determine the course of treatment (Gordon, 2009).
Numerous “lotions and potions” have been suggested for the prevention and management of radiodermatitis, such as ascorbic acid, vitamin D, aloe vera, chamomile and calendula creams, and almond ointment. Other common practices include avoiding zinc and aluminum based creams and deodorants, wearing loose cotton clothing, and applying non-adhesive dressings (Harper, Franklin, Jenrette, & Aguero, 2004). However, there is limited scientific data to support these recommendations (Kassab, Cummings, Berkovitz, Van Haselen, & Fisher, 2009). The following recommendations are based on the best current evidence, including a meta-analysis of 28 randomized controlled trials by the Supportive Care Guidelines Group (SCGG) (Bolderston, Lloyd, Wong, Holden, & Robb-Belnderman, 2006). The approach to the management of radiodermatitis should be based on the severity of symptoms and patient comfort.
Mild erythema is best managed by washing gently with a mild soap or shampoo (Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006). Washing reduces bacterial load and risk for infection (Hymes, Strom, & Fife, 2006). In fact, mild soap and water has been found to be more effective in the prevention and treatment of radiodermatitis than topical aloe vera (Richardson, Smith, McIntyre, Thomas, & Pilkington, 2005). Contrary to popular belief, the use of deodorant during radiation therapy does not increase a patient’s risk for radiodermatitis (Theberge, Harel, & Dagnault, 2009).
The management of dry desquamation should aim to moisturize the area and to minimize patient discomfort. A non-scented, hydrophilic, lanolin-free cream may be used for the treatment of dry desquamation and/or the prevention of moist desquamation (Harper, Franklin, Jenrette, & Aguero, 2004; Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006). There is also some evidence to suggest that topical steroids may be beneficial. Topical steroids inhibit the up-regulation of cytokines in response to radiation. A randomized control trial by Bostrom et al. (2001) tested prophylactic corticosteroid cream and emollient cream versus placebo cream during radiotherapy and for three weeks following the completion of therapy. A significantly lower frequency of radiodermatitis was found in the corticosteroid group, which suggests that topical steroids may prevent radiodermatitis. The SCGG supports the use of a low-dose topical corticosteroid to relieve itching and irritation (Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006). However, topical creams should be discontinued if moist desquamation develops (Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006). The guidelines also do not recommend the use of sucralfate, Biafine, ascorbic acid, aloe vera, chamomile cream, almond ointment, or polymer adhesive skin sealant for the prevention or treatment of radiodermatitis due to insufficient evidence (Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006).
Hydrocolloid or hydrogel dressings, with or without moisturizing cream, have traditionally been used in the management of moist desquamation in order to promote a moist environment for reepithelization (Hymes, Strom, and Fife, 2006; Harper, Franklin, Jenrette, & Aguero, 2004). Hydrogels have been found to be superior to gentian violet in the healing of moist desquamation (Gollins, Gaffney, Slade, & Swindell, 2008). However, a recent study that compared hydrogel versus dry dressing on the healing time of moist desquamation found that healing time was significantly prolonged in the hydrogel group (Macmillian et al., 2007). A possible explanation for this finding is that while a moist environment dose promote wound healing, too much moisture leads to maceration. In response, several small case-studies have trialed thinner dressings made of silicone (MacBride, Wells, Hornsby, Sharp, Finnila, & Downie, 2008) or hydrocolloid (Russi, Merlano, Comino, & Numico, 2007). Preliminary data suggests that thinner dressings are safe and well tolerated, but larger randomized controlled trials are needed to evaluate the efficacy of these dressings (MacBride et al.; Russi et al.). The SCGG also determined that there is insufficient evidence to recommend a particular type of dressing for the management of moist desquamation (Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006). The SCGG did not make recommendations for when to modify or hold radiotherapy due to severe radiodermatitis (Bolderston, Lloyd, Wong, Holden, & Robb-Benderman, 2006). Therefore, the decision to modify or hold radiotherapy should be make in accordance with institution guidelines, if applicable, and at the discretion of the radiation oncologist.
Radiodermatitis is a common side effect of radiotherapy that is associated with pain, decreased quality of life, and treatment delays that may compromise the effectiveness of radiation treatment (McQuestion, 2006; Fisher et al., 2000; Hymes, Strom, & Fife 2006). Radiodermatitis ranges from mild to severe and may be acute or chronic in nature. The management of radiodermatitis should be based on the severity of symptoms, as determined by RTOG or NCI grade, and should promote wound healing and patient comfort. At a minimum, research indicates that all patients should be allowed to shower, with mild soap and water, and to use deodorant.
Oncology nurses play a critical role in the assessment and management of radiodermatitis. However, D’haese, Bate, Claes, Boone, Vanvoorden, & Efficace (2005) found that there is wide discrepancy between nursing interventions for the prevention and management of radiodermatitis. A possible explanation for this finding is that there is a paucity of evidence to support traditional interventions for radiodermatitis.
The SCGG guidelines also reinforce the need for additional research in the prevention and management of radiodermatitis. Unfortunately, the SCGG was unable to comment on the efficacy of several potential interventions due to insufficient evidence. Larger randomized controlled trials with standardized assessment tools are needed to allow researchers to compare research findings between interventions. Important topics within radiodermatitis include pain management, quality of life, and wound healing. Specifically addition research is needed to make informed suggestions regarding various topical creams and dressings. As demonstrated by D’haese et al. (2005), in addition to stronger randomized controlled trials, research results must be disseminated and translated into nursing practice.
Table 1: RTOG Radiation Morbidity Scoring
Table 2: NCI Radiation Toxicity
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