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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 2  |  Issue : 1  |  Page : 8-12

A study of clinical patterns of acute radiation dermatitis among patients attending dermatology outpatient department at tertiary center in Western India


Department of Dermatology, Venereology and Leprosy, Goa Medical College, Bambolim, Goa, India

Date of Web Publication5-Jan-2018

Correspondence Address:
Varadraj Pai
Department of Dermatology, Goa Medical College, Bambolim, Goa
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/CDR.CDR_17_17

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  Abstract 


Background: Radiation dermatitis (RD) is a commonly encountered adverse effect of definitive radiation therapy. The severity of RD is influenced by multiple patient and treatment-related factors. Radiation depletes the basal cell layer of skin and initiates a complex sequence of events leading to dose-dependent acute or late sequelae. The management of RD requires a multidisciplinary approach. Objectives: The aim is to highlight the pattern and the profile of patients with acute RD attending dermatology outpatient department. Materials and Methods: Hospital-based cross-sectional study of 47 consecutive adult patients with acute RD attending skin outpatient department over a period of 12 months. Results: A total of 47 patients of RD attended the skin clinic, of which were 16 males and 31 were female. The RD was reported within the first 2 weeks of initiation of therapy in most of the patients. Grade 1 RD was the least common presentation. Conclusions: This study highlights the importance of grading the RD, for the appropriate management of the patients suffering from the same and is also a step toward the prevention of the RD.

Keywords: Acute radiation dermatitis, radiation dermatitis, radiotherapy


How to cite this article:
Saini S, Pai V, Shukla P, Ranglani H. A study of clinical patterns of acute radiation dermatitis among patients attending dermatology outpatient department at tertiary center in Western India. Clin Dermatol Rev 2018;2:8-12

How to cite this URL:
Saini S, Pai V, Shukla P, Ranglani H. A study of clinical patterns of acute radiation dermatitis among patients attending dermatology outpatient department at tertiary center in Western India. Clin Dermatol Rev [serial online] 2018 [cited 2018 Aug 18];2:8-12. Available from: http://www.cdriadvlkn.org/text.asp?2018/2/1/8/222265




  Introduction Top


Radiotherapy (RT) forms an integral component of management in oncology, and approximately three-fourth of patients diagnosed with cancer receive RT during their treatment.[1] Skin reactions are the most common acute toxicity which are seen in patients undergoing RT and can be a limiting factor in patient's compliance to therapy.[1] Among cancer patients receiving radiation therapy, 95% will develop some form of radiodermatitis, including erythema, dry desquamation, and moist desquamation.[2]

Radiation-induced skin toxicities can be classified as acute and delayed complications. Acute cutaneous reactions usually occur within 90 days of radiotherapy.[3] Radiation works by damaging both benign and malignant clonogenic cells. The cells which are highly proliferative and sufficiently oxygenated are the most radiosensitive. The most radiosensitive organ systems are bone marrow, reproductive and gastrointestinal systems, skin, muscle, and brain. Tissues with a rapid turnover, such as the epidermis and mucosal endothelium, therefore show radiation damage soon after treatment, and this is called acute reaction. The incidence and severity of acute radiation dermatitis (RD) depend on multiple patient and treatment-related factors.[3],[4] Although isolated reports on the patterns and therapeutic approach in acute RD are available, studies on the pattern of RD in Indian patients are lacking.


  Materials and Methods Top


The study was hospital-based cross-sectional and was conducted over a period of 12 months among patients visiting the Department of Dermatology. All patients who presented with complaints of skin lesion following a radiotherapy treatment or 3–4 weeks after completion of radiotherapy were included in the study. Patients suffering from other lesions such as fungal infection or changes that were noted after 1 month of completion of therapy were excluded from the study. A detailed history was elicited, and thorough clinical examination was done on every patient. The findings were recorded in a specially prepared pro forma after obtaining informed consent. Photographic records of the clinical lesions were maintained. The physical examination was conducted after fully exposing the involved site in adequate light with gloved hands. Patients were graded clinically according to the classification of RD from the National Cancer Institute common terminology criteria for adverse events version 3.[3] Relevant investigations pertaining to the study were carried out which included potassium hydroxide mount, Grams staining, Tzanck smear, swabs for culture and sensitivity and ELISA for HIV testing.

All the patients included in the study were given adequate treatment which included emollients and topical steroids for dry desquamation, and topical or systemic antibiotics with dressing for wet desquamation with regular follow-up.


  Results Top


During the study period of 12 months, total of 262 patients were given radiotherapy, of which 47 (17.9%) patients developed acute RD and formed the part of our study.

Out of the 47 patients with acute RD, 16 (34%) were male and 31 (64%) were female. The age of the patients ranged from 40 to 70 years. Maximum number of patients were in above 50 years (63.8%) [Figure 1]. Carcinoma cervix accounted for maximum number of cases (36%). According to the site of involvement, most cases of RD in head and neck malignancies presented as Grade 1–2 while breast carcinoma presented with Grade 2 and cervix carcinoma as Grade 3–4 [Figure 2],[Figure 3],[Figure 4],[Figure 5]. Most patients (74.4%) developed RD within one to 2 weeks of starting radiotherapy [Figure 6]. All patients with Ca prostate developed RD followed by 70% of Ca hypopharynx cases [Figure 7]. Although Grade 1 was the least common type of presentation, overall no significant difference was seen among various grades of RD [Table 1].
Figure 1: Distribution of cases with respect to age and sex

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Figure 2: Distribution of cases of radiation dermatitis as per the grading and the site of involvement

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Figure 3: Grade 1 radiation dermatitis over the forearms presenting as dull erythema and desquamation

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Figure 4: Grade 3 radiation dermatitis over the neck presenting as confluent desquamation with hyperpigmentation

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Figure 5: Grade 4 radiation dermatitis over the genitals presenting as ulceration and necrosis over the groin

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Figure 6: Onset of radiation dermatitis after radiotherapy

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Figure 7: Percentage of patients with specific malignancies developing radiation dermatitis

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Table 1: Distribution of patients with respect to grade of radiation dermatitis

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  Discussion Top


RD can be classified into acute RD, chronic RD, radiation recall dermatitis, eosinophilic, polymorphic, and pruritic eruption of radiotherapy and radiation-induced dermatoses.[5]

Acute radiation effect is defined as changes occurring within 2–3 weeks of starting radiation and continuing 3–4 weeks after completion of RT.[5],[6] The aim of RT is to maximize the therapeutic ratio by optimizing the dose to the target tissue while minimizing the damage to the adjacent structures.[7],[8]

Acute RD is a frequent side-effect of fractionated external radiotherapy which affects the patients' quality of life and may cause cessation or prolongation of radiation period.[4],[7],[8] Radiation-induced skin toxicities can be classified as acute and delayed complications. Acute radiation-induced skin toxicities include erythema, edema, dry and wet desquamation, ulceration, necrosis, and hemorrhage. These may be accompanied by itching and/or pain and are related to a variety of patient and treatment-related factors [Table 2].[4]
Table 2: Factors affecting radiation dermatitis

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Early changes reflect injury, apoptosis and reproductive failure in germinative epidermal and hair matrix cells, reduced division rates in surviving cells, and vascular damage.[5] Radiation-induced skin changes appear to be due to impairment of epidermal permeability barrier function since these changes are associated with an increase in transepidermal water loss (TEWL). The functional damage to the stratum corneum induced by the ionizing radiation occurs with a delayed course, starting within a mean period of 11 days and reaching maximal values after a mean period of 27 days (range, 13–75 days). The onset of TEWL increase precedes the onset of RD and the maximal TEWL measurements precede the peak of skin changes. Patients with an early onset of TEWL increase show a longer duration of skin symptoms.[5],[9]

Radiation exposure causes depletion of basal epithelial layers of skin. It also induces an inflammatory and a vascular response with extracapillary cell injury and capillary dilation.[7],[8] Pigmentary changes are caused by increased melanin production by melanocytes and the migration of melanin to the more superficial layers of the epidermis.[7] The exposure of the subdermal lymphatics as a result of the loss of the superficial epithelium leads to moist desquamation, or after higher doses, skin necrosis. Similar damage caused to the epithelial lining of hair follicles causes hair loss. Telangiectasia results from excessive loss of microvascular endothelium, causing capillary loops to contract and fuse into dilated channels beneath an atrophied epidermis.[1],[10] RD differs from radiation burn wherein the later there is instantaneous structural damage and damage starts in the superficial layers and progresses deeper with the severity of the injury. In RD, the adjacent irradiated tissue also suffers from anatomical and physiological change leading to impaired graft uptake.[1],[10]

Cutaneous changes in RD vary with a dose of radiation. Epilation occurs at an approximate dose of 20 Gy. Hyperpigmentation and dry desquamation occur after 45 Gy. Moist desquamation can be seen at 50–60 Gy dose. Radiation doses above 60 Gy lead to further necrosis.[1],[7] A regular wound healing occurs in a phased manner involving hemostasis and inflammation, followed by proliferation and maturation.[1]

Grading of RD is given in [Table 3]. The Radiation Therapy Oncology Group/European Organization for Research and Treatment of Cancer score is an objective criteria-based scale that assesses toxicities in tissues and organs and is followed most commonly by radiation oncologists worldwide for reporting of radiation-related acute and late effects.[11]
Table 3: Grading of radiation dermatitis

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In this study, 17.9% of the patients presented with acute RD predominantly seen in females (64%), whereas in the study by Porock and Kristjanson, the overall incidence of acute erythematous reactions of 80%–90% has been reported.[12] While moist desquamation (Grade 2 and 3) is seen in around 10%–15% of the patients undergoing RT to radical doses in the study by Porock and Kristjanson, there was not much difference in the various grades of RD.[12] These differences in the incidence may be due to the skin color and the attitude of the treating population where minimal erythema may not be appreciated and ignored.

Bonner et al. in their study found that majority of patients undergoing radiotherapy for head and neck cancers experience mild to moderate (Grade 1–2) RD, which is similar to the findings in this study.[13] Archambeau et al.[14] noted that higher doses of fractionated radiation above 50–60 Gy may lead to moist desquamation while radiation doses above 60 Gy may lead to further damage leading to radionecrosis similar to our study. Moist desquamation or ulceration of the irradiated chest wall/breast skin (Grade 3–4) toxicity has been reported in 20%–25% of patients receiving radiotherapy to the breast.[15] Grade 3 and Grade 4 accounted for 33% of the cases of the RD in patients with breast cancer in our study.

Histopathologically, acute RD is characterized by scattered pyknotic keratinocytes and epidermal edema.[16] In subacute RD, there is interface dermatitis with basal vacuolar change and apoptotic keratinocytes. In the late stages, the epidermis may be atrophic with the loss of the normal rete ridge pattern and the development of focal basal vacuolar change. Eosinophilic homogenized sclerosis of the dermal collagen is seen. Pilosebaceous structures are lost, but the arrector pili muscles remain, in contrast to the changes following thermal burns, when they are lost.[17]

The natural history of the acute reaction cannot be modified, but one can avoid making the reaction worse. Patients are advised to leave the area open to the air as far as possible.[18] The general consensus is that a majority of the patients do not need specific therapy and are best treated symptomatically. General measures such as cleansing with low pH gentle cleanser, avoiding irritation, extremes of temperature, and friction are followed. Erythema is treated with emollients. Dry desquamation also requires emollients and gentle cleansing. The use of topical steroids is controversial. Moist desquamation is treated with hydrogel or hydrocolloid dressing, burn pads or foam dressing for exudative wounds. Topical and systemic antibiotic following bacterial culture, if necessary. In chronic ulcer in addition to the above measures, careful debridement using mechanical, enzymatic, autolytic, and bio-surgical methods are used. Other treatment modalities include hyperbaric oxygen, pentoxifylline, amifostine, and zinc supplements.[3]


  Conclusions Top


Acute RD is the most common side effect of definitive radiotherapy encountered in this study, as it depletes the basal cell layer of skin and initiates a complex sequence of events leading to necrosis and late complications. Therefore, it necessitates active intervention by a multidisciplinary group to manage both acute and late effects of radiation therapy on the skin and the subcutaneous tissues.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Khanna NR, Kumar DP, Laskar SG, Laskar S. Radiation dermatitis: An overview. Indian J Burns 2013;21:24-31.  Back to cited text no. 1
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2.
Singh M, Alavi A, Wong R, Akita S. Radiodermatitis: A review of our current understanding. Am J Clin Dermatol 2016;17:277-92.  Back to cited text no. 2
    
3.
Hymes SR, Strom EA, Fife C. Radiation dermatitis: Clinical presentation, pathophysiology, and treatment 2006. J Am Acad Dermatol 2006;54:28-46.  Back to cited text no. 3
    
4.
Omidvari S, Saboori H, Mohammadianpanah M, Mosalaei A, Ahmadloo N, Mosleh-Shirazi MA, et al. Topical betamethasone for prevention of radiation dermatitis. Indian J Dermatol Venereol Leprol 2007;73:209.  Back to cited text no. 4
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5.
Ali SY, Reddy MH, Hussain SF. Cutaneous effects of radiotherapy – A review article. Innov J Med Health Sci 2014;4:341-9.  Back to cited text no. 5
    
6.
Carper E, McGuire M, Boland N. Head and neck cancer nursing. In: Harrison LB, Sessions RB, Hong WK, editors. Head and Neck: A Multidisciplinary Approach. 1st ed. New York: Lippincott Raven Publishers; 1999. p. 179-95.  Back to cited text no. 6
    
7.
Archambeau JO, Shymko RM. Tissue population configuration as a modifier of organ dose response. Int J Radiat Oncol Biol Phys 1988;15:727-34.  Back to cited text no. 7
    
8.
Ratliff C. Impaired skin integrity related to radiation therapy. J Enterostomal Ther 1990;17:193-8.  Back to cited text no. 8
    
9.
Schmuth M, Sztankay A, Weinlich G, Linder DM, Wimmer MA, Fritsch PO, et al. Permeability barrier function of skin exposed to ionizing radiation. Arch Dermatol 2001;137:1019-23.  Back to cited text no. 9
    
10.
Denham JW, Hauer-Jensen M. The radiotherapeutic injury – A complex 'wound'. Radiother Oncol 2002;63:129-45.  Back to cited text no. 10
    
11.
Hoeller U, Tribius S, Kuhlmey A, Grader K, Fehlauer F, Alberti W. Increasing the rate of late toxicity by changing the score? A comparison of RTOG/EORTC and LENT/SOMA scores. Int J Radiat Oncol Biol Phys 2003;55:1013-8.  Back to cited text no. 11
    
12.
Porock D, Kristjanson L. Skin reactions during radiotherapy for breast cancer: The use and impact of topical agents and dressings. Eur J Cancer Care (Engl) 1999;8:143-53.  Back to cited text no. 12
    
13.
Bonner JA, Harari PM, Giralt J, Azarnia N, Shin DM, Cohen RB, et al. Radiotherapy plus cetuximab for squamous-cell carcinoma of the head and neck. N Engl J Med 2006;354:567-78.  Back to cited text no. 13
    
14.
Archambeau JO, Pezner R, Wasserman T. Pathophysiology of irradiated skin and breast. Int J Radiat Oncol Biol Phys 1995;31:1171-85.  Back to cited text no. 14
    
15.
Pignol JP, Olivotto I, Rakovitch E, Gardner S, Sixel K, Beckham W, et al. A multicenter randomized trial of breast intensity-modulated radiation therapy to reduce acute radiation dermatitis. J Clin Oncol 2008;26:2085-92.  Back to cited text no. 15
    
16.
Junkins-Hopkins JM. Disorders associated with physical agents: Heat, cold, radiation and trauma. In: Elder DE, editor. Levers's Histopathology of Skin. 10th ed. New Delhi: Lippincott Williams and Wiliams; 2009. p. 348-52.  Back to cited text no. 16
    
17.
Weedon D. Reaction to physical agents. In: Weedon's Skin Pathology. 3rd ed. London: Churchill Livingstone Elsevier: Elsevier 2010. p. 528-9.  Back to cited text no. 17
    
18.
Kelly CG, Peat I. Radiotherapy and reactions to ionizing radiation. In: Burn T, Breatnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8th ed. London: Wiley-Blackwell Publishing; 2010. p. 79.1- 79.19.  Back to cited text no. 18
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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