INTRODUCTION
Among the most common side effects, radiation dermatitis (RD) affects up to 95% of patients receiving radiotherapy,1 significantly impacting the quality of life of those affected and leading to poor medication compliance.2 Acute RD occurs within 90 days of beginning treatment. It may initially present as mild, transient erythema, before progressing to persistent erythema or hyperpigmentation associated with pruritic scaly skin (dry desquamation); tender erythematous skin accompanied by serous exudate, hemorrhagic crusting and possible bullae (moist desquamation) develops in over 30% of patients,3 and may evolve into full-thickness ulceration or necrosis (Figure 1).1 The degree of severity of RD depends on multiple risk factors. Patient-related risk factors include, but are not limited to, age, sex, smoking, poor nutritional status, high body mass index, comorbid conditions, ultraviolet exposure, and Staphylococcus aureus colonization.1,4 Treatment-related factors include total radiation dose, dose fractionation schedule, concurrent chemotherapy, the site of treatment, and the volume and surface area of irradiated tissue.1 Notably, RD occurs with increased frequency in patients being treated for sarcoma, breast, anal, vulva, and head and neck cancers due to the proximity of the radiation target to the skin.1 Intensity-modulated radiotherapy significantly improves dose distribution compared with conventional radiation therapy and has been shown to reduce the occurrence of moist desquamation, which is associated with increased pain and reduced quality of life.5
Pathogenesis
Radiation-induced DNA damage impairs the mitotic processes of stem cells in the basal layer of the skin, reducing the capacity to regenerate the epidermis and promoting cellular senescence in keratinocytes. Pro-inflammatory cytokines and chemokines recruit neutrophils to the irradiated skin, exacerbating inflammation and inducing reactive hyperplasia, causing structural dysfunction of the epidermal barrier.6 Evolving data suggests that S. aureus may play a role in the pathogenesis of RD. S. aureus produces exogenous erythrotoxins and expresses superantigens --- which have the capacity to activate T-cells and promote a robust inflammatory sequela.4 Like processes occurring with atopic dermatitis, it is thought that inflammation disrupts the skin barrier, making the skin susceptible to microbial colonization, propelling inflammation, and preventing re-epithelialization of keratinocytes exposed to radiation.4 A recent cohort study supported the association between S. aureus colonization and RD, demonstrating that the prevalence of baseline nasal S. aureus colonization was higher among patients with breast or head and neck cancer who developed grade 2 or higher RD compared with those who developed grade 1 RD (34.5% vs 12.8%; P=0.2 by X2 test).7
Prevention and Management
There is currently no gold standard treatment for RD, though recommendation guidelines on the best prevention and management strategies of acute RD given the current evidence following a four-round Delphi consensus process have recently been published.8 For prevention of acute RD, the following 6 interventions reached consensus (75% or greater) to recommend: polyurethane film (Hydrofilm), mometasone, betamethasone, and olive oil, and specifically photobiomodulation or low-level laser therapy and silicone-based polyurethane (Mepitel film) in patients with breast cancer.8 The use of silver sulfadiazine (SSD) reached near-consensus supporting recommendation (60-74%) for prevention of acute RD due to insufficient evidence. Conflicting evidence exists for the utility of SSD in managing wound healing and infections in burn wounds. Clinically, non-silver dressings have been found to be as effective as SSD9 and an in vivo study using a full-thickness burn mouse model found treatment with SSD delayed wound closure and reduced expression of proinflammatory cytokines integral to wound healing.10 For the management of acute
