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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 .

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What s under your skin l.jpg
WHAT’SUNDER 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 l.jpg

Objectives

Explain effects of external beam radiationtherapy.

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.


Directions l.jpg
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


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RADIATION

SKIN STRUCTURE AND FUNCTION

GENETICS

BREAST SKIN CHANGES

INFLAMMATION

NURSING CARE AND PATIENT EDUCATION


Radiation l.jpg
RADIATION

Microsoft Office Clip Art 2007


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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


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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


Radiation8 l.jpg
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


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Radiation Direct Effect

  • DNA absorbs radiation

  • The atoms become ionized and damaged

  • Less common than indirect damage

    Microsoft Office Clip Art 2007


Radiation indirect effect l.jpg
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 l.jpg
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 damage12 l.jpg
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


Radiation13 l.jpg
Radiation

CONTROLS CANCER CELLS BY

  • Inducing apoptosis

  • Causing permanent cell cycle arrest or terminal differentiation

  • Inducing cells to die of mitotic catastrophe


Apoptosis l.jpg
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 l.jpg
Cell Cycle

www.wikigenetics.org/images/4/4b/Cell_cycle1.jpg


Cell cycle death terminal differentiation denucleation l.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 l.jpg
Radiation Effects

Radiosensitive

Radioresistant

Cells that do not divide regularly or at all and are highly differentiated

Examples are muscle cells and nerve cells

  • Cells renewing rapidly with little or no differentiation

  • Examples are skin cells, mucous membranes, and hematopoietic stem cells


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Radiation Effects

Radiosensitive

Radioresistant

Late effects

Damage months or years after first exposure

Permanent

Damage becomes more severe as time goes on

Dependent upon dose-time-volume factors

  • Acute effects

  • Damage within weeks to months of exposure

  • Temporary

  • Normal cells affected are capable of repair

  • Dependent upon dose-time-volume factors


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Radiation Effects

Radiosensitive

Radioresistant

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

  • 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


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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


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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


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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

    Microsoft Office

    Clip Art 2007


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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.


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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.


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Wrong answer, try again.

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

Click here to return to question



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GENETICS in the treated area only.

Microsoft Office Clip Art 2007


Slide28 l.jpg

Chromosome: in the treated area only.rod-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


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GENE: in the treated area only.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 l.jpg
Radiation effect on genes in the treated area only.

  • 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


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Genetics in Radiation in the treated area only.

  • 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


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Genetics in Radiation in the treated area only.

  • 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


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Genetics in Radiation in the treated area only.

  • 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


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Genetics in Radiation in the treated area only.

  • 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


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p53 Tumor Suppressor Gene in the treated area only.

  • 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


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Genetics in Radiation in the treated area only.

  • 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


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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


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Wrong answer, try again. mutated or lost?

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


Correct p 53 l.jpg
Correct! p 53 mutated or lost?


Inflammation l.jpg
INFLAMMATION mutated or lost?

Microsoft Office Clip Art 2007


Inflammation41 l.jpg
Inflammation mutated or lost?

  • 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 l.jpg
Five Cardinal Signs of Inflammation mutated or lost?

  • Redness

  • Swelling

  • Heat

  • Pain

  • Loss of function

    Microsoft Office Clip Art 2007


Acute inflammation l.jpg
Acute Inflammation mutated or lost?

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


Vascular stage l.jpg
Vascular Stage mutated or lost?

  • 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 stage45 l.jpg
Vascular Stage mutated or lost?

  • 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 stage46 l.jpg
Vascular Stage mutated or lost?

  • 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


Cellular stage l.jpg
Cellular Stage mutated or lost?

  • 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 l.jpg
Cellular Stage: Granulocytes mutated or lost?

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.


Segmented neutrophils l.jpg
Segmented Neutrophils mutated or lost?

http://upload.wikimedia.org/wikipedia/commons/2/29/S


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Cellular Stage: Monocytes mutated or lost?

  • 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.


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Phases of Acute Inflammation Response mutated or lost?

MARGINATION

Leukocytes increase adhesion molecules,

slow migration, and move along periphery of blood vessels


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Phases of Acute Inflammation Response mutated or lost?

EMIGRATION

Leukocytes pass through capillary walls and migrate into tissue spaces


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Phases of Acute Inflammation Response mutated or lost?

CHEMOTAXIS

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


Phases of acute inflammation response54 l.jpg
Phases of Acute Inflammation Response mutated or lost?

PHAGOCYTOSIS

Neutrophils and macrophages engulf and degrade bacteria and debris

Phagocytosis

http://upload.wikimedia.org/.../180px-Phagocytosis2. png


Inflammatory mediators l.jpg

Inflammatory Mediators mutated or lost?

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


Inflammation with chemical mediator l.jpg
Inflammation with Chemical Mediator mutated or lost?

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 l.jpg
Inflammation with Chemical Mediators mutated or lost?

INFLAMMATORY

RESPONSE

Tissue Damage

CHEMICAL

MEDIATOR

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


Inflammation with chemical mediators58 l.jpg
Inflammation with Chemical Mediators mutated or lost?

INFLAMMATORY

RESPONSE

Pain

CHEMICAL

MEDIATOR

Prostaglandins

Bradykinins


Inflammation with chemical mediator59 l.jpg
Inflammation with Chemical Mediator mutated or lost?

INFLAMMATORY

RESPONSE

Leukocytosis

CHEMICAL

MEDIATOR

Interleukin-1

Other Cytokines


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What are the five major signs of inflammation? mutated or lost?

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


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Wrong answer, try again. mutated or lost?

Click here to return to question



Skin structure and function l.jpg
SKIN STRUCTURE AND FUNCTION function.

Microsoft Office Clip Art 2007


Slide64 l.jpg
SKIN function.

  • Largest organ of the body

  • Receives approximately one-third of heart’s oxygenated blood

  • Body’s FIRST defense mechanism


Slide65 l.jpg
Skin function.

Three Layers

  • Epidermis (outer layer)

  • Dermis (middle layer)

  • Subcutaneous tissue (inner layer)

    Microsoft Office Clip Art 2007


Skin structure l.jpg
Skin Structure function.

http://upload.wikipedia.org/wiki/File:Skin/common/3/34/Skin/jpg.


Epidermis l.jpg
Epidermis function.

  • 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


Epidermal layers l.jpg
Epidermal Layers function.

  • 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


Layers of epidermis l.jpg
Layers of Epidermis function.

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


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Terminal Transition in Epidermis function.

  • 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)


Dermis l.jpg
Dermis function.

  • 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


Subcutaneous tissue l.jpg
Subcutaneous Tissue function.

  • 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 l.jpg
Functions of Skin function.

  • 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


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Skin function.

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)


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What is the major function of the skin? function.

A. Vitamin D Production

B. Sensory perception.

C. Regulation of body temperature.

D. Protection


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Wrong answer, try again. function.

Click here to return to picture



Breast skin changes l.jpg
BREAST SKIN CHANGES function.

Microsoft Office Clip Art 2007


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Radiation Changes function.

  • 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 changes80 l.jpg
Radiation Changes function.

  • 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 changes81 l.jpg
Radiation Changes function.

  • 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 changes82 l.jpg
Radiation Changes function.

  • 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)


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Dry Desquamation function.

  • 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 desquamation84 l.jpg
Dry Desquamation function.

Adapted with permission by Nature Publishing Group: Leukemia, volume 17, issue 7, 2003.

www. Nature.com/leu/journal/v17/n7images/240991f1.jpg


Moist desquamation l.jpg
Moist Desquamation function.

  • 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 desquamation86 l.jpg
Moist Desquamation function.

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


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Acute Skin Reactions function.

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 reactions88 l.jpg
Acute Skin Reactions function.

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 reactions89 l.jpg
Acute Skin Reactions function.

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 reactions90 l.jpg
Acute Skin Reactions function.

MOIST DESQUAMATION

Bright erythema

Sloughing skin

Exposed dermis

Serous exudate

Pain


Acute skin reactions91 l.jpg
Acute Skin Reactions function.

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 l.jpg
Late Skin Reactions function.

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 l.jpg
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 l.jpg
Sorry, wrong answer. dry, flaking, and peeling skin?

Click here to return to question


Yes dry desquamation l.jpg
Yes! Dry desquamation. dry, flaking, and peeling skin?


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NURSING CARE AND PATIENT EDUCATION dry, flaking, and peeling skin?

Microsoft Office Clip Art 2007


Nursing care l.jpg
Nursing Care dry, flaking, and peeling skin?

  • 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.


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Patient Instructions dry, flaking, and peeling skin?

  • 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


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Patient Instructions dry, flaking, and peeling skin?

  • 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.


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Patient Instructions dry, flaking, and peeling skin?

  • 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 instructions101 l.jpg
Patient Instructions dry, flaking, and peeling skin?

  • 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 l.jpg
Breast Skin Products dry, flaking, and peeling skin?

Cleanser and moisturizer

Given to every breast cancer patient being treated with radiation

Have patients use twice a day


Breast skin products103 l.jpg
Breast Skin Products dry, flaking, and peeling skin?

Healing ointment and skin protectant

Used for dry desquamation

Apply to affected area


Breast skin products104 l.jpg
Breast Skin Products dry, flaking, and peeling skin?

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 l.jpg
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 l.jpg
Sorry, incorrect. Try again. patient?

Click here to return to the question



Case study l.jpg
Case Study affected area.

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 study109 l.jpg
Case Study affected area.

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.


References l.jpg
References affected area.

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

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