Transcript Skin Care of Breast Cancer Patients Undergoing Standard External

WHAT’S 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 @ aol.com
dmbraunreiter @ wi.rr.com
Objectives
1. Explain effects of external beam radiation
therapy.
2. Briefly describe genetic mechanisms involved
in radiation.
3. Summarize the acute physiologic
mechanisms of inflammation.
4. Describe the structure and function of skin.
5. Identify breast skin changes after radiation
treatment.
6. Review nursing care for breast cancer
patients undergoing radiation therapy.
Directions
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RADIATION
SKIN STRUCTURE
AND FUNCTION
GENETICS
BREAST SKIN
CHANGES
INFLAMMATION
NURSING CARE
AND PATIENT
EDUCATION
RADIATION
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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
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
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
Radiation Direct Effect
• DNA absorbs radiation
• The atoms become ionized and damaged
• Less common than indirect damage
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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
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
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
Radiation
CONTROLS CANCER CELLS BY
1. Inducing apoptosis
2. Causing permanent cell cycle arrest or
terminal differentiation
3. Inducing cells to die of mitotic catastrophe
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
Cell Cycle
www.wikigenetics.org/images/4/4b/Cell_cycle1.jpg
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
Radiation Effects
Radiosensitive
• Cells renewing rapidly with
little or no differentiation
• Examples are skin cells,
mucous membranes, and
hematopoietic stem cells
Radioresistant
• Cells that do not divide
regularly or at all and are
highly differentiated
• Examples are muscle cells
and nerve cells
Radiation Effects
Radiosensitive
• Acute effects
• Damage within weeks to
months of exposure
• Temporary
• Normal cells affected are
capable of repair
• Dependent upon dose-timevolume factors
Radioresistant
• Late effects
• Damage months or years
after first exposure
• Permanent
• Damage becomes more
severe as time goes on
• Dependent upon dose-timevolume factors
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
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
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
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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
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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.
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.
Wrong answer, try again.
Radiation only affects the area being treated
and causes damage to DNA.
Click here to return
to question
Correct! Radiation causes the
reproductive death of cells in the
treated area only.
GENETICS
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Chromosome:
rod-shaped molecule of DNA threaded around proteins containing
specific genes that carry hereditary information
Histones 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
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/geneinchromosome.jpg
Radiation effect on genes
1. Ionizing radiation causes phosphorylation of
histone H2AX (forming gamma-H2AX)
2. Reaction dependent on ataxia telangiectesia
mutated (ATM) molecule
3. 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
Genetics in Radiation
4. Next, phosphorylating the ATM protein
amplifies the damage signal
5. And recruits proteins critical for repair, such
as the BRCA1 and HDAC4
6. Which allows a G2 cycle checkpoint
7. 53BP1 important in double-strand DNA
damage sensing, repair, and tumor
suppression
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
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
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
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
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
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
Wrong answer, try again.
EGFR is epidermal growth factor, Ras is a protooncogene, and p21 is a protein influenced by
p53 and acts as a stop signal in the cell cycle.
Click here to return to
question
Correct! p 53
INFLAMMATION
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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).
Five Cardinal Signs of Inflammation
1.
2.
3.
4.
5.
Redness
Swelling
Heat
Pain
Loss of function
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Acute Inflammation
Two major components
1. VASCULAR
2. 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).
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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
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
Vascular Stage
1. FIRST is immediate transient response
2. SECOND is immediate sustained response
which occurs with more serious injury and
continues for several days and damages
vessels in the area
3. THIRD is a delayed hemodynamic response,
which increases capillary permeability that
occurs 4 to 24 hours after injury, seen with
RADIATION types of injuries
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
Cellular Stage: Granulocytes
Granulocytes divided into three types
neutrophils, eosinophils, and basophils.
1. Neutrophils are primary phagocytes; arrive
within 90 minutes to injury site; contain
enzymes and antibacterial substances that
destroy and degrade engulfed particles.
Segmented Neutrophils
http://upload.wikimedia.org/wikipedia/commons/2/29/S
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.
Phases of Acute Inflammation
Response
MARGINATION
Leukocytes increase adhesion molecules,
slow migration, and move along periphery of
blood vessels
Phases of Acute Inflammation
Response
EMIGRATION
Leukocytes pass through capillary walls and
migrate into tissue spaces
Phases of Acute Inflammation
Response
CHEMOTAXIS
Leukocytes in tissues guided by cytokines,
bacteria, and cell debris
Phases of Acute Inflammation
Response
PHAGOCYTOSIS
Neutrophils and macrophages engulf and
degrade bacteria and debris
Phagocytosis
http://upload.wikimedia.org/.../180px-Phagocytosis2. png
Inflammatory Mediators
CYTOKINES
Polypeptide products of various cell typesmostly 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
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)
Inflammation with Chemical Mediators
INFLAMMATORY
RESPONSE
Tissue Damage
CHEMICAL
MEDIATOR
Lysomomal enzymes
and products released
from neutrophils,
macrophages, and
other inflammatory
cells
Inflammation with Chemical Mediators
INFLAMMATORY
RESPONSE
CHEMICAL
MEDIATOR
Pain
Prostaglandins
Bradykinins
Inflammation with Chemical Mediator
INFLAMMATORY
RESPONSE
CHEMICAL
MEDIATOR
Leukocytosis
Interleukin-1
Other Cytokines
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
D. Redness, swelling, heat, pain, and loss of function
Wrong answer, try again.
Click here to return
to question
Correct! Redness, swelling, heat,
pain, and loss of function.
SKIN STRUCTURE AND
FUNCTION
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SKIN
• Largest organ of the body
• Receives approximately one-third of heart’s
oxygenated blood
• Body’s FIRST defense mechanism
Skin
Three Layers
• Epidermis (outer layer)
• Dermis (middle layer)
• Subcutaneous tissue (inner layer)
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Skin Structure
http://upload.wikipedia.org/wiki/File:Skin/common/3/34/Skin/jpg.
Epidermis
1. Multi-layered and impermeable
2. Outer layer that forms a resistant cover and
permeability barrier of varying thickness
3. Renews itself continuously through cell
division in deepest (basal) layer
4. Undergoes keratinization to produce scales
that are shed from outer layer
5. Avascular and receives nutrients from dermis
Epidermal Layers
1. Stratum corneum is outermost layer
composed of flattened dead cells and is
about 25% of total thickness
2. Stratum granulosum is thin transitional layer
3. Stratum spinosum (squamous cell) is viable
layer made up of mainly post-mitotic cells
4. Basal cell layer is viable and deepest layer
where majority of cell division occurs
Layers of Epidermis
http://en.wikipedia.org/wiki/Image:Gray941.png
Terminal Transition in Epidermis
1. Half the cells produced in basal layer undergo
mitosis
2. After dividing, cells leave basal cell layer and
enter stratum spinosum and then stratum
granulosum
3. This is where the cells flatten, lose
organelles, and become mature, keratininized
cells of the stratum corneum
4. Cells detach and desquamate, but are
continually replaced by cells produced in
basal layer (turnover process is 30 days)
Dermis
1.
2.
3.
4.
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
5. Interacts with epidermis during wound repair
Subcutaneous Tissue
1.
2.
3.
4.
5.
Composed mostly of adipose tissue
Cushion to physical trauma
Insulator to temperature change
Energy reservoir
Nerves, blood vessels, and lymphatics run
through it
Functions of Skin
1.
2.
3.
4.
5.
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)
6. Excretion
Skin
First line of defense
against bacteria and
foreign substances,
physical trauma,
heat, or rays
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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)
What is the major function of the
skin?
A. Vitamin D Production
B. Sensory perception.
C. Regulation of body temperature.
D. Protection
Wrong answer, try again.
Click here to
return to picture
Correct! Protection.
BREAST SKIN CHANGES
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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
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
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
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)
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
Dry Desquamation
Adapted with permission by Nature Publishing Group: Leukemia, volume 17, issue 7, 2003.
www. Nature.com/leu/journal/v17/n7images/240991f1.jpg
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
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
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
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
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
Acute Skin Reactions
MOIST DESQUAMATION
Bright erythema
Sloughing skin
Exposed dermis
Serous exudate
Pain
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
Late Skin Reactions
PHOTOSENSITIVITY
Enhanced erythema over skin exposed to UV
radiation from sun and tanning bed/booths
Begins during treatment and is lifelong
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
Sorry, wrong answer.
Click here to return
to question
Yes! Dry desquamation.
NURSING CARE AND PATIENT
EDUCATION
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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 patient’s present
skin condition, preexisting skin disorders, medical
conditions, medications, age-related factors, and
nutritional status.
• Consistency in assessment and documentation is
important.
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
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.
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.
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.
Breast Skin Products
Cleanser and moisturizer
Given to every breast cancer patient being
treated with radiation
Have patients use twice a day
Breast Skin Products
Healing ointment and skin protectant
Used for dry desquamation
Apply to affected area
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
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.
Sorry, incorrect. Try again.
Click here to return
to the question
Yes! Apply cleanser and
moisturized twice a day to the
affected area.
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
nurse’s actions and interventions?
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.
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Good Job
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