WHAT

1
WHATS UNDER YOUR SKIN?

• Skin Care of Breast Cancer Patients Undergoing
  Standard External Beam Radiation
• Donna M. Braunreiter RN BSN OCN
• MSN Student
• Alverno College
• Spring 2009, MSN 621
• dmbraunreiter _at_ aol.com
• dmbraunreiter _at_ wi.rr.com

2
Objectives

• Explain effects of external beam radiation
  therapy.
• Briefly describe genetic mechanisms involved in
  radiation.
• Summarize the acute physiologic mechanisms of
  inflammation.
• Describe the structure and function of skin.
• Identify breast skin changes after radiation
  treatment.
• Review nursing care for breast cancer patients
  undergoing radiation therapy.

3
Directions

• To move to the next slide, click this
• To move to the previous slide, click this
• To return to the beginning, click this
• To return to the topics section, click this

4
RADIATION
SKIN STRUCTURE AND FUNCTION
GENETICS
BREAST SKIN CHANGES
INFLAMMATION
NURSING CARE AND PATIENT EDUCATION
5
RADIATION

• 
  Microsoft
  Office Clip Art 2007

6
Radiation Treatment

• Skin reaction is the most common side effect
  during breast cancer radiation treatments
• Over 90 of women receiving radiation for breast
  cancer will develop some skin changes during
  their course of treatment

7
Radiation

• Interacts with all biological materials in its
  path
• Direct and indirect damage to cells causes DNA
  changes
• Causes many molecular responses that induce
  cellular mechanisms for DNA repair, cell cycle
  arrests, and apoptosis

8
Radiation

• Major effect on dividing cells is reproductive
  death
• Leaves cells unable to reproduce
• Radiosensitivity of cell determines degree of
  injury and when it will happen

9
Radiation Direct Effect

• DNA absorbs radiation
• The atoms become ionized and damaged
• Less common than indirect damage
• 
  
• 
  Microsoft Office
  Clip Art 2007

10
Radiation Indirect Effect

• Water molecules surrounding DNA are ionized
• Creates highly reactive free radicals such as
  hydroxyl radicals, peroxide, hydrated electrons,
  and oxygen radicals
• These radicals interfere with DNA and cause
  damage and strand breakage
• Common because 80 of a cell is water

11
Radiation Damage

• Direct and indirect damage break bonds in DNA
  backbone
• Results in loss of base, nucleotide, or one or
  both strands of DNA
• Single-strand DNA breaks are repaired using the
  opposite strand as a template
• Can result in mutation if not repaired correctly

12
Radiation Damage

• Double-strand DNA breaks related to cell killing
• Results in mitotic death
• X-rays are sparsely ionizing and
  cause locally clustered damage
• Leads to clinically significant
  events
• 
  
  
  
  
  
• 
  
  
  
• 
  
  
  
  
  
• 
  
  
  DNA Structure
  
  
  
  
• 
  
  
  United States National Library of
  Medicine
• 
  
  http//ghr.nlm.nih.gov/
  handbook/illustrations.dnastructure.jpg
  

13
Radiation

• CONTROLS CANCER CELLS BY
• Inducing apoptosis
• Causing permanent cell cycle arrest or terminal
  differentiation
• Inducing cells to die of mitotic catastrophe

14
Apoptosis

• Programmed cell death
• Radiation damage triggers signaling cascades
  which causes cell self-destruct mechanisms
• Characteristics are nucleus fragmentation and
  blebbing
• Tumors undergoing apoptosis have good clinical
  response

15
Cell Cycle

• www.wikigenetics.org/images/4/4b/C
  ell_cycle1.jpg

16
Cell Cycle Death/Terminal Differentiation
(Denucleation)

• Cells can arrest in any phase of cell cycle
• Radiation damage mainly in G1 and G2 phases
• Normal cells and cancer cells retaining p53
  function block in G1
• Cancer cells with p53 loss or mutation block in
  G2 phase
• G2 arrest related to cellular repair of DNA
  radiation-induced DNA damage

17
Radiation Effects

• Radiosensitive

• Radioresistant

• Cells renewing rapidly with little or no
  differentiation
• Examples are skin cells, mucous membranes, and
  hematopoietic stem cells

• Cells that do not divide regularly or at all and
  are highly differentiated
• Examples are muscle cells and nerve cells

18
Radiation Effects

• Radiosensitive

• Radioresistant

• Acute effects
• Damage within weeks to months of exposure
• Temporary
• Normal cells affected are capable of repair
• Dependent upon dose-time-volume factors

• Late effects
• Damage months or years after first exposure
• Permanent
• Damage becomes more severe as time goes on
• Dependent upon dose-time-volume factors

19
Radiation Effects

• Radiosensitive

• Radioresistant

• Higher doses over shorter periods of time to
  larger volumes of tissues result in more severe
  acute reactions
• Acute damage results from depletion of actively
  proliferating parenchymal or stromal cells
• Characteristics are vascular dilation, local
  edema, and inflammation

• Severity of late effects more dependent upon
  total dose delivered and volume if tissue
  irradiated
• Damage to endothelial cells or connective tissues
  results in late effects occurring as a result of
  narrowing or occlusion of small vasculature and
  fibrosis

20
Radiation Effects

• Acute and late side effects from radiation
  therapy are LOCAL and ONLY affect tissues
  receiving treatment
• Presence and severity of acute effects can not
  predict late effects of radiation
• Late reactions such as tissue necrosis or dense
  tissue fibrosis can occur independently of acute
  reactions

21
SUPINE POSITION

• Most common position for breast cancer radiation
  therapy
• MUST be used if lymph nodes need to be treated
• May involve radiation exposure to heart, lungs,
  ribs, and contralateral breast
• 
  
  
  Microsoft Office Clip Art 2007

22
PRONE POSITION

• Used for women with larger pendulous breast,
  cardiac and/or pulmonary comorbidities
• Possible improved dose homogeneity
• Potential reduction in lung and heart irradiation
• Microsoft Office
• Clip Art 2007

23
Patient-Related Considerations

• Normal age-related changes
• thinning of the epidermis and dermis,
• diminished elasticity,
• decreased dermal turgor,
• which results in delayed healing.
• Nutritional status is also important for healing.

24
What is the effect of radiation on cells?
A. Reproductive death of cells throughout the
body
B. Reproductive death of cells in the treated
area only
C. Radiation skin reactions cause internal
injuries.
D. Radiation helps repair DNA damage.
25
Wrong answer, try again.

• Radiation only affects the area being treated and
  causes damage to DNA.

Click here to return to question
26
Correct! Radiation causes the reproductive death
of cells in the treated area only.
27
GENETICS

• 
  Microsoft Office
  Clip Art 2007

28
Chromosomerod-shaped molecule of DNA threaded
around proteins containing specific genes that
carry hereditary informationHistones are
proteins that act as spools around which DNA
winds, as compaction is necessary to large genes
inside cell nuclei histones also function as
gene regulators

• United States
  National Library of Medicine
  http//ghr.nlm.nih.gov/handbook/illustrations
  /chromosomestructure.jpg

29
GENE
biological unit of hereditary segment of DNA
needed to contribute to a function and specifies
a trait

• United States
  Library of Medicine
• http//ghr.nlm.nih.gov/handbook/illustrations/ge
  neinchromosome.jpg

30
Radiation effect on genes

• Ionizing radiation causes phosphorylation of
  histone H2AX (forming gamma-H2AX)
• Reaction dependent on ataxia telangiectesia
  mutated (ATM) molecule
• Followed by accumulation of 53BP1, a protein
  acting as central mediator for critical pathways,
  including phosphorylating (which conveys the DNA
  damage signal to) tumor suppressor protein p53

31
Genetics in Radiation

• Next, phosphorylating the ATM protein amplifies
  the damage signal
• And recruits proteins critical for repair, such
  as the BRCA1 and HDAC4
• Which allows a G2 cycle checkpoint
• 53BP1 important in double-strand DNA damage
  sensing, repair, and tumor suppression

32
Genetics in Radiation

• HR (homologous repair) efficient in late S or G2
  phase when sister chromatids have replicated but
  not separated
• Repair is cell cycle dependent
• Undamaged homologous chromosome or sister
  chromatid or replicated chromosome is used as a
  template to fill in missing DNA sequences in
  damaged chromosome

33
Genetics in Radiation

• Human tumor cells block in G2 after DNA
  double-strand damage, when repairs are
  detectible, and irradiation induced G2 checkpoint
  allows more time for cells to undergo HR
  (homologous repair) and survive radiation

34
Genetics in Radiation

• NHEJ (nonhomologous endjoining) is where blunt
  ends of chromosomes severed by radiation are
  directly rejoined
• Less cell cycle dependent
• Highly mutagenic due to template-free rejoining
  lacks specificity of HR
• Ends of different chromosomes can be rejoined,
  leading to chromosomal aberrations or expression
  of dangerous fusion proteins

35
p53 Tumor Suppressor Gene

• p53 stops activity of tumors
• Loss or mutation of p53 predisposes to cancer
• (e.g. inheriting only one functional copy of
  p53 gene from parents)
• p53 protein binds DNA and stimulates another gene
  to produce protein p21 and blocks next stage of
  cell division
• Mutant p53 no longer binds DNA and does not
  interact with p21
• Results in p21 unable to act as a stop signal
• Cells divide uncontrollably

36
Genetics in Radiation

• Ras, Raf, and EGFR alter cellular sensitivity to
  radiation, but exact mechanisms unknown
• Ras is a proto-oncogogene (portion of DNA that
  regulates normal cell proliferation and repair)
• Raf is a gene coding for protein kinase
• EGFR (epidermal growth factor receptor) found on
  surface of some cells and where epidermal growth
  factor binds, causing the cells to divide

37
What is a common gene that can lead to many
cancers it is mutated or lost?
A. EGFR
B. p 21
C. p 53
D. Ras
38
Wrong answer, try again.

• EGFR is epidermal growth factor, Ras is a
  proto-oncogene, and p21 is a protein influenced
  by p53 and acts as a stop signal in the cell
  cycle.

Click here to return to question
39
Correct! p 53
40
INFLAMMATION

• 
  Microsoft Office
  Clip Art 2007

41
Inflammation

• Reaction of vascularized tissue to local injury.
• Causes are many and varied.
• Commonly it results from an immune response to
  infection organisms.
• Other causes are trauma, surgery, caustic
  chemicals, extremes of heat and cold, and
  ischemic damage to body tissues.
  (Porth, 2005).

42
Five Cardinal Signs of Inflammation

• Redness
• Swelling
• Heat
• Pain
• Loss of function
• 
  Microsoft Office Clip Art 2007
  
  
  
  

43
Acute Inflammation

• Two major components
• VASCULAR
• CELLULAR
• Inflammatory mediators, acting together or
  in sequence, amplify the initial response and
  influence its evolution by regulating the
  subsequent vascular and cellular responses
  (Porth, 2005).
• 
  
  
• 
  
  
  Microsoft Office
• 
  
  Clip Art
  2007

44
Vascular Stage

• Constriction of small blood vessels in injured
  area
• Vasoconstriction followed rapidly by vasodilation
  of the arterioles and venules
• Causes the area to becomes congested and results
  in redness and warmth

45
Vascular Stage

• Capillary permeability increases causes swelling,
  pain, and impaired function
• Movement of fluid from capillaries into
  interstitial spaces (swelling) dilutes the
  offending agent
• Extravasation of plasma proteins into
  extracellular spaces causes exudate
• Blood stagnation and clotting of blood in the
  capillaries around the injury site aids in
  localizing the spread of infectious microorganisms

46
Vascular Stage

• FIRST is immediate transient response
• SECOND is immediate sustained response which
  occurs with more serious injury and continues for
  several days and damages vessels in the area
• THIRD is a delayed hemodynamic response, which
  increases capillary permeability that occurs 4 to
  24 hours after injury, seen with RADIATION types
  of injuries

47
Cellular Stage

• Movement of phagocytic white blood cells
  (leukocytes) into area of injury
• Two types of leukocytes involved--granulocytes
  and monocytes
• Requires the release of chemical mediators from
  sentinel cells (mast cells and macrophages)
  already positioned in tissues

48
Cellular Stage Granulocytes

• Granulocytes divided into three types
  
• neutrophils, eosinophils, and basophils.
• Neutrophils are primary phagocytes arrive within
  90 minutes to injury site contain enzymes and
  antibacterial substances that destroy and degrade
  engulfed particles.

49
Segmented Neutrophils

• http//upload.wikimedia.org/wikip
  edia/commons/2/29/S

50
Cellular Stage Monocytes

• Mononuclear phagocytes are largest of white blood
  cells
• Last 3 to 4 times longer than granulocytes and
  survive longer in the tissues.
• Help to destroy agent, aid in signaling processes
  of specific immunity, and help to resolve
  inflammatory process.
• Arrive by 24 hours and at 48 hours monocytes and
  macrophages are predominant cells at injury site
• Engulf larger and greater quantities of foreign
  materials and migrate to lymph nodes.

51
Phases of Acute Inflammation Response

• MARGINATION
• Leukocytes increase adhesion molecules,
• slow migration, and move along periphery of
  blood vessels

52
Phases of Acute Inflammation Response

• EMIGRATION
• Leukocytes pass through capillary walls and
  migrate into tissue spaces

53
Phases of Acute Inflammation Response

• CHEMOTAXIS
• Leukocytes in tissues guided by cytokines,
  bacteria, and cell debris

54
Phases of Acute Inflammation Response

• PHAGOCYTOSIS
• Neutrophils and macrophages engulf and degrade
  bacteria and debris
• 
  
  Phagocytosis
• 
  
• http//upload.wikimedia.o
  rg/.../180px-Phagocytosis2. png

55
Inflammatory Mediators

• CYTOKINES
• Polypeptide products of various cell types-
  
• mostly lymphocytes and macrophages
• modulate functions of other cell types
• COLONY-STIMULATING FACTORS
• directs growth of immature marrow precursor cells
• INTERLEUKINS
  (Ils)
• INTERFERONS (Ifs)
• TUMOR NECROSIS FACTOR

56
Inflammation with Chemical Mediator

• INFLAMMATORY
• RESPONSE
• Swelling, redness, and
• tissue warmth
• (vasodilation and increased capillary
  permeability)

• CHEMICAL
• MEDIATOR
• Histamine (fast acting and causes dilatation
  and increased permeability of capillaries),
• Prostaglandins,
• Leukotrienes,
• Bradykinin,
• Platelet-activating factor
• (attracts neutrophils)

57
Inflammation with Chemical Mediators

• INFLAMMATORY
• RESPONSE
• Tissue Damage

• CHEMICAL
• MEDIATOR
• Lysomomal enzymes and products released from
  neutrophils, macrophages, and other inflammatory
  cells

58
Inflammation with Chemical Mediators

• INFLAMMATORY
• RESPONSE
• Pain

• CHEMICAL
• MEDIATOR
• Prostaglandins
• Bradykinins

59
Inflammation with Chemical Mediator

• INFLAMMATORY
• RESPONSE
• Leukocytosis

• CHEMICAL
• MEDIATOR
• Interleukin-1
• Other Cytokines

60
What are the five major signs of inflammation?
A. Redness, pus, fever, pain, and swelling
B. Pain, swelling, numbness, tingling, and cold

C. Heat, pain, swelling, pus, and loss of
function
C. Heat, pain, swelling, pus, and loss of
function
D. Redness, swelling, heat, pain, and loss of
function
61
Wrong answer, try again.
Click here to return to question
62
Correct! Redness, swelling, heat, pain, and loss
of function.
63
SKIN STRUCTURE AND FUNCTION

• 
  Microsoft Office Clip Art
  2007

64
SKIN

• Largest organ of the body
• Receives approximately one-third of hearts
  oxygenated blood
• Bodys FIRST defense mechanism

65
Skin

• Three Layers
• Epidermis (outer layer)
• Dermis (middle layer)
• Subcutaneous tissue (inner layer)
• 
  Microsoft Office Clip Art 2007

66
Skin Structure

• http//upload.wikipedia.org/wiki/FileSkin
  /common/3/34/Skin/jpg.

67
Epidermis

• Multi-layered and impermeable
• Outer layer that forms a resistant cover and
  permeability barrier of varying thickness
• Renews itself continuously through cell division
  in deepest (basal) layer
• Undergoes keratinization to produce scales that
  are shed from outer layer
• Avascular and receives nutrients from dermis

68
Epidermal Layers

• Stratum corneum is outermost layer composed of
  flattened dead cells and is about 25 of total
  thickness
• Stratum granulosum is thin transitional layer
• Stratum spinosum (squamous cell) is viable layer
  made up of mainly post-mitotic cells
• Basal cell layer is viable and deepest layer
  where majority of cell division occurs

69
Layers of Epidermis

• http//en.wikipedia.org/wiki/Image
  Gray941.png

70
Terminal Transition in Epidermis

• Half the cells produced in basal layer undergo
  mitosis
• After dividing, cells leave basal cell layer and
  enter stratum spinosum and then stratum
  granulosum
• This is where the cells flatten, lose
  organelles, and become mature, keratininized
  cells of the stratum corneum
• Cells detach and desquamate, but are continually
  replaced by cells produced in basal layer
  (turnover process is 30 days)

71
Dermis

• Tough and durable middle layer 1-3mm thick
• Gives skin strength, elasticity, and softness
• Protects deeper structures from injury
• Contains blood vessels that regulate body
  temperature and provide nourishment to epidermis
  also contains nerves, hair follicles and various
  glands
• Interacts with epidermis during wound repair

72
Subcutaneous Tissue

• Composed mostly of adipose tissue
• Cushion to physical trauma
• Insulator to temperature change
• Energy reservoir
• Nerves, blood vessels, and lymphatics run through
  it

73
Functions of Skin

• PROTECTION - MOST IMPORTANT!
• Regulation of body temperature
• Sensory perception
• Vitamin D production
• Provides an active system of immunologic defense
  (dermal lymphocytes, mast cells, mononuclear
  phagocytes, Langerhans cells)
• Excretion

74
Skin

• First line of defense against bacteria and
  foreign substances, physical trauma,
• heat, or rays
• Microsoft Office Clip Art 2007

• Protection works by
• (1) eccrine gland sweating
• (2) insulation by the skin and subcutaneous
  tissue
• (3) regulation of cutaneous blood flow
  (vasoconstriction and
• vasodilation)
• (4) muscle activity
• (shivering)

75
What is the major function of the skin?
A. Vitamin D Production
B. Sensory perception.
C. Regulation of body temperature.
D. Protection
76
Wrong answer, try again.
Click here to return to picture
77
Correct! Protection.
78
BREAST SKIN CHANGES

• 
  Microsoft Office Clip Art 2007

79
Radiation Changes

• Reflect injury occurring mostly in the epidermis
• Primary target for acute radiation skin reactions
  is the basal cell layer
• Entire epidermis turns over in 30 days

80
Radiation Changes

• Early erythema within few hours after radiation
  and subsides after 24-48 hours
• Inflammatory response from histamine-like
  substances that cause dermal edema from the
  permeability and dilatation of capillaries

81
Radiation Changes

• Main erythematous reaction occurs 3-6 weeks after
  radiation begins and is due to a varying severity
  loss of epidermal basal cells
• Basal cell density changes with higher doses of
  radiation
• Reddening of the skin due to a secondary
  inflammatory reaction or hyperemia

82
Radiation Changes

• Higher radiation doses reduce number of mitotic
  cells and increase in degenerate cells
• When cells are not being reproduced at the same
  rate in the basal cell layer and the normal
  migration of cells to stratum corneum continues,
  epidermis is denuded in time equal to natural
  turnover (30 days)

83
Dry Desquamation

• If enough numbers of clonogenic cells (cells
  giving rise to a clone of cells) remain to
  replace injured cells, there is atypical
  thickening of the stratum corneum
• The populations of the basal-layer stem cells
  become depleted in the radiation treated area
• This can result in dry flaking, scaling, and
  itching in the treated area

84
Dry Desquamation

• Adapted with permission by Nature Publishing
  Group Leukemia, volume 17, issue 7, 2003.
  
  
• www. Nature.com/leu/journa
  l/v17/n7images/240991f1.jpg

85
Moist Desquamation

• If new cell proliferation is inadequate, there is
  exposed dermis with oozing of serum
• Repopulation of the basal cell layer of epidermis
  after irradiation is mainly from surviving
  clonogenic cells (cells giving rise to a clone of
  cells) within the irradiated area
• If the treated area is completed denuded of
  clonogenic epithelial cells, then healing results
  from division and migration of viable cells from
  skin around the irradiated area

86
Moist Desquamation

• Used with permission , Adapted from Ostomy Wound
  Management , volume 51, issue 10, Managing
  Radiation Skin Injury
• www.o-wm/com/article/4752/files/photos
  /notesfig19867.gif

87
Acute Skin Reactions

• ERYTHEMA
• Redness that outlines treatment field and
  intensifies as treatment continues
• Increased skin temperature
• Edema
• Follows after 2-3 weeks after standard
  fractionated radiation and resolves 20-30 days
  after last treatment

88
Acute Skin Reactions

• DRY DESQUAMATION
• Dryness
• Flaking
• Peeling
• Pruritus
• Following 3-4 weeks of standard fractionated
  radiation and resolves 1-2 weeks after completion
  of treatments

89
Acute Skin Reactions

• HYPERPIGMENTATION
• Tanned appearance
• Following 2-3 weeks of standard fractionated
  therapy and is usually resolved in 3 months to 1
  year after treatment but may be chronic

90
Acute Skin Reactions

• MOIST DESQUAMATION
• Bright erythema
• Sloughing skin
• Exposed dermis
• Serous exudate
• Pain

91
Acute Skin Reactions

• MOIST DESQUAMATION
• Can occur with radiation or with trauma or
  friction and most recovery usually 2-4 weeks
  after completion of treatment
• SKIN REGROWTH
• New skin is smooth, pink, thin, and dryer
• Depends upon severity but usually is complete 2-3
  months after therapy

92
Late Skin Reactions

• PHOTOSENSITIVITY
• Enhanced erythema over skin exposed to UV
  radiation from sun and tanning bed/booths
• Begins during treatment and is lifelong

93
What develops after 3 -4 weeks of radiation with
symptoms of dry, flaking, and peeling skin?
A. Dry desquamation
B. Erythema
C. Moist desquamation
D. Hyperpigmentation
94
Sorry, wrong answer.
Click here to return to question
95
Yes! Dry desquamation.
96
NURSING CARE AND PATIENT EDUCATION

• 
  Microsoft Office Clip Art 2007

97
Nursing Care

• Perform skin assessment before radiation
  treatments, at least weekly during treatments,
• 1 month following completion of treatment,
  and each follow-up appointment.
• Initial assessment includes the patients present
  skin condition, preexisting skin disorders,
  medical conditions, medications, age-related
  factors, and nutritional status.
• Consistency in assessment and documentation is
  important.

98
Patient Instructions

• Use gentle soaps ONLY, such as Dove or Ivory,
  which do not contain additives
• Use a moisturizing lotion on the treatment area
  twice a day
• Expose the treated area to the air as much as
  possible
• Do not wear underwire bras
• Do not wear tight-fitting clothing that rubs or
  binds underneath the breast

99
Patient Instructions

• Wear a comfortable bra. Wear cotton t-shirts
  underneath your bra to absorb moisture.
• Drink 8-10 glasses of water a day.
• Eat well-balanced meals and maintain your weight
  during treatment.
• Continue with your normal daily activities.

100
Patient Instructions

• Sexual activity may continue during treatment.
  You are not radioactive and there are no dangers
  to your partner.
• Avoid extreme temperatures to the affected area.
  Do not use water bottles, heating pads, sun
  lamps, ice bags, etc.
• Avoid exposing your skin to the sun, as the sun
  and sun rays are an additional form of radiation
  to the skin. Always apply sunscreen with SPF or
  15 before sun exposure.

101
Patient Instructions

• Do not apply tape or adhesive bandages to the
  treated area.
• Speak with your nurse about deodorant use
• Continue with the range of motion exercises for
  your arm and shoulder.
• Report any pain or swelling to your doctor or
  nurse.

102
Breast Skin Products

• Cleanser and moisturizer
• Given to every breast cancer patient being
  treated with radiation
• Have patients use twice a day

103
Breast Skin Products

• Healing ointment and skin protectant
• Used for dry desquamation
• Apply to affected area

104
Breast Skin Products

• MOIST DESQUAMATION
• Topical aluminum acetate packets (astringent)
  mixed with normal saline
• Gently debride area and apply solution to area
  for 20 minutes rewet every 10 minutes and repeat
  once a day
• Apply hydrocolloid dressing over affected area
  and secure
• Do NOT use hydrocolloid dressing 4 hours before
  treatment

105
What is the recommended treatment for every
radiation patient?
A. Soap and water once a day
B. Apply cleanser and moisturizer twice a day on
the affected area
C. Apply a hydrocolloid over the treated area
D. Encourage daily sun exposure.
106
Sorry, incorrect. Try again.
Click here to return to the question
107
Yes! Apply cleanser and moisturized twice a day
to the affected area.
108
Case Study

• Mrs. K is a breast cancer patient who has
  received radiation to her left breast for the
  past 4 weeks. She is complaining of increasing
  pain and her left breast is bright red in color,
  with sloughing skin and a serous exudate.
• What is the name of this skin condition
  caused by radiation? What would be the nurses
  actions and interventions?

109
Case Study

• Moist desquamation.
• The nurse would apply an aluminum acetate
  solution for 20 minute and gently debride the
  area.
• A hydrocolloid dressing would then be placed over
  this area and secured.
• The patient would be given instructions about
  this treatment once a day.
• Pain management will be addressed.

110
References

• Abeloff, M.D., Armitage, J. O., Niederhuber, J.
  E., Kastan, M. B., McKenna, W. G.
• (2004). Clinical oncology (3rd ed.).
  Philadelphia, PA Elsevier, Inc.
• Bruner, D. W., Bucholtz, J. D., Iwamoto, R.,
  Strohl, R. (Eds.) (1998). Manual for
• radiation oncology nursing practice and
  education. Pittsburgh, PA Oncology
• Nursing Society.
• Fox, S. I. (1996). Human physiology (5th ed.).
  Dubuque, IA Wm. C. Brown Publishers.
• Groenwald, S.L., Frogge, M.H., Goodman, M.,
  Yarbro, C.H. (1993). Cancer nursing Principles
  and practice (3rd ed.). Boston, MA Jones
  Bartlett.
• Hill, S. (2008). Managing radiation skin injury.
  Ostomy Wound Management, 51(10),
• 1-2. Retrieved May 13, 2009, from,
  http//www.o-wn.com/article/4752.
• Mahon, S. M. (Ed.). (2007). Breast cancer.
  Pittsburgh, PA Oncology Nursing Society.
• Milojkovic, D., Short, K., Salisbury, J. R.,
  creamer, D., du Vivier a. W. P., Mufti, G. J.
  (2003). Dose-limiting dermatological toxicity
  secondary to imatinib mesylate
• (STI571) in chronic myeloid leukaemia.
  Leukemia, (17), 1414-1416. Retrieved May 13,
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Good Job

• 
  
  Microsoft Office Clip Art 2007