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Wound and Integument Lecture NURS 3005 Spring 2015

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Wound and Integument Lecture NURS 3005 Spring 2015
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SKIN CARE AND WOUND PREVENTION By: Karen C. Lyon, PhD, APRN, ACNS, NEA Presented by: Wanda Butaud RN, BSN, WOCN Spring 2015
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Page 1: Wound and Integument Lecture NURS 3005 Spring 2015

SKIN CARE AND WOUND PREVENTION

By: Karen C. Lyon, PhD, APRN, ACNS, NEAPresented by: Wanda Butaud RN, BSN, WOCN

Spring 2015

Page 2: Wound and Integument Lecture NURS 3005 Spring 2015

Differentiate categories of chronic wounds in terms of predisposing factors, anatomic location and wound characteristics

Describe assessment parameters for venous ulcers, diabetic leg/foot ulcers and pressure ulcers

Describe wound care management strategies including appropriate primary and secondary dressings, compression, offloading, biologic dressings and bed surfaces

http://guidelines.gov/content.aspx?id=24492

Student Learning Outcomes

Page 3: Wound and Integument Lecture NURS 3005 Spring 2015

Chronic Wound Prevalence in US

Over 6.5 million patients with chronic wounds in US

One half of these are pressure sores80% of patients with pressure sores are over

65 years of age85% of paraplegics will develop a pressure

sore63% of pressure sores are present at hospital

admission

Over $25 billion spent annually on treatment

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810192/

http://www.justice.gov/opa/pr/2003/June/03_civ_386.htm

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A wound is a disruption of normal anatomic structure and function that is usually inclusive

of the skin.

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◦Anatomic continuity◦Function

Wound healing should result in restoration of…

Page 6: Wound and Integument Lecture NURS 3005 Spring 2015

ACUTE

VS.CHRONIC

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Shear is caused by tissue layers sliding against each other. This results in disruption or angulation of blood vessels, usually at the fascia level

Purple areas on sacrum and heels Ulcers start deep and work outward Irregularly shaped Undermined

Shear

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Excessive moisture causes maceration which acts as a factor in skin breakdown

Incontinence Wound drainage Excessive sweating

Moisture

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Altered skin integrity Delayed wound healing Decreased resistance to infection Nutritional supplements Feeding tubes Anabolic steroids

Nutritional Compromise

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Activity and mobility Loss of sensation Age Disease states Previous ulcers Medications

Contributing Factors

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KEY Cells Macrophages Fibroblasts Endothelial Cells

KEY Elements Macrophage derived

- PDGF- TGF-- FGF-2 (bFGF)

MMPs- Cell migration

Granulation Tissue Formation

Reference: Monaco JL, Lawrence TL. Acute wound healing; an overview. Clinics in Plastic Surgery 30 (2003): 1-12.

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Reepithelialization

Keratinocyte Proliferation

Keratinocyte Migration

Relevant Growth Factors

Keratins

Page 13: Wound and Integument Lecture NURS 3005 Spring 2015

Chronic wounds have failed to proceed through an orderly and

timely process to produce anatomic and functional integrity, or proceeded

through the repair process without establishing a sustained anatomic

and functional result.Lazarus GS et al. Arch Dermatol 1994.

Page 14: Wound and Integument Lecture NURS 3005 Spring 2015

It is not as much an issue of time as it is condition of the wound

What we are really talking about is wound healing failure which may be identifiable almost at the time of injury

Chronic is actually a misnomer:

Page 15: Wound and Integument Lecture NURS 3005 Spring 2015

Ischemia Infection Edema Scarring Radiation injury

Topical steroids Local toxins Trauma, pressure Foreign bodies Local malignancy

Local factors affecting wound healing:

Page 16: Wound and Integument Lecture NURS 3005 Spring 2015

Diabetes mellitus Tobacco use Renal failure Nutritional

deficiencies Hereditary disorders Alcohol use Distant malignancy Systemic infections

Connective tissue disease

Immunological disorders

Chemotherapeutic agents

Extremes of age Systemic steroids Hepatic failure

Systemic factors affecting wound healing:

Page 17: Wound and Integument Lecture NURS 3005 Spring 2015

0

1000

2000

3000

4000

5000

6000

7000

8000

9000

10000

11000

Num

ber

of C

ells

0 1 2 3 4 5 6 7 8 9 10 11 12 13

Day

OA

YA

NB

(Buras and Buras, Harvard Medical School, MGH, Boston)

Age associated differences in cellular proliferation…

Page 18: Wound and Integument Lecture NURS 3005 Spring 2015

5

10

15

20

25

30

35

# C

ells

X 1

04

1 2 3 4 5 6 7 8 9

Non-Diabetic

Diabetic

Days

(Buras and Buras, Harvard Medical School, MGH, Boston)

Decreased cellular proliferation with diabetes…

Page 19: Wound and Integument Lecture NURS 3005 Spring 2015

A PRESSURE ULCER IS:Any lesion caused by unrelieved pressureResults in damage to underlying tissueLocated over bony prominences

PRESSURE ULCER DEFINITION

Page 20: Wound and Integument Lecture NURS 3005 Spring 2015

Pressure Ulcers

• External pressure impedes local blood flow to skin (20mmHg), muscle• Muscle and subcutaneous tissue more susceptible to injury than skin• Necrosis generally over bony

prominence• Loss of skin moisture

Pathophysiology

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Stage 1

Stage 2

Stage 3Stage 4

Page 25: Wound and Integument Lecture NURS 3005 Spring 2015

Posterior Calf

Heel 8%

Sacrum 23%

Elbow 3% Spinous

processes 1%

Scapula 5%

Back of head 1%

Dorsum of foot and ankle

Knee 6%

Thigh Iliac crest 4%

Anterior Chest

Acromion process

Cheek and ear

Page 26: Wound and Integument Lecture NURS 3005 Spring 2015

Points of PressureLateral Position

Malleolus 7% Medial and lateral condyles

Greater trochanter 15%

Ribs Ear

Page 27: Wound and Integument Lecture NURS 3005 Spring 2015

Points of PressureSitting Position

Plantar surface of foot

Scapula

Sacrum & coccyxIschial tuberosity 24%

Heel

Popliteal

Page 29: Wound and Integument Lecture NURS 3005 Spring 2015

Venous Leg Ulcers

• Prolonged venous hypertension• Valvular incompetence, DVT, calf muscle dysfunction• Enlarged dermal capillaries, reduced capillary number, microvascular thrombosis, increased permeability of microlymphatics• WBC sequestration,

ischemic/reperfusion injury

Pathophysiology

Page 30: Wound and Integument Lecture NURS 3005 Spring 2015
Page 31: Wound and Integument Lecture NURS 3005 Spring 2015

Diabetic Wounds/Amputations

Pathophysiology • Sensory, motor, autonomic neuropathy • Low resistance to infection with attenuated inflammatory response impaired chemotaxis, inefficient bacterial killing• Perivascular localization of

albumin• Large vessel arterial occlusive disease• Peripheral A-V shunting

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Table 1. Suggested Technique for the Management of Chronic Wounds

Intervention Handwashing Gloves

Supplies (Includes solutions and dressing supplies) Instruments

Wound cleansing Yes Clean

Normal saline solution or commercially prepared wound cleanser - sterile; maintain as clean per care setting policy*

Irrigation with sterile device; maintain as clean per care setting policy

         Routine dressing change without debridement Yes Clean

Sterile; maintain as clean per care setting policy*

Sterile; maintain as clean per care setting policy

         Dressing change with mechanical, chemical, or enzymatic debridement Yes Clean

Sterile; maintain as clean per care setting policy*

Sterile; maintain as clean per care setting policy

         Dressing change with sharp, conservative bedside debridement Yes Sterile Sterile Sterile

* "Maintain clean as per care setting policy" means that each care setting must address the parameters for maintenance,

such as expiration dates for supplies, consideration of cost, and correct interpretation of the manufacturer's recommendations.        

Page 44: Wound and Integument Lecture NURS 3005 Spring 2015
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Page 47: Wound and Integument Lecture NURS 3005 Spring 2015

Farrow Wraps

Page 48: Wound and Integument Lecture NURS 3005 Spring 2015
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Skin careRisk assessment

Pressure relief/reduction

Nutritional

Support

Early

Treatment

Education

Outcomes

Tracking

Documentation

NURSING IMPLICATIONS


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