The Science of

Wound Bed Preparation

Becky Adkins, RN, MSN, CWS

Nurse Practitioner

April 28, 2004

Objectives

• Differentiate normal wound healing from

chronic wound healing

• Discuss factors that contribute to

impaired healing in the the chronic wound

• Identify the components of Wound Bed

Preparation to include debridement,
bacterial burden, moisture balance
Components of Normal Wound
Healing
Cell types involved

Coagulation Platelets
Process
Platelets
Macrophages
Inflammatory Neutrophils
Process
Macrophages
Migratory/ Lymphocytes
Fibroblasts
Proliferative Epithelial cells
Process Endothelial cells

Remodeling Fibroblasts
Process

Injury/Hours/Days Weeks
23Kane DP, Krasner D. In: Chronic Wound Care. 2nd ed. Health Management Publications Inc; 1997:1-4.
 Chronic Wound
Repeated Trauma
Local Tissue Ischemia Delayed Healing
Necrotic Tissue
Heavy Bacterial Burden
Tissue Breakdown Prolonged Inflammation
Stimulation of macrophage and
neutrophils to wound bed

Release of pro-inflammatory
Degrades ECM cytokines
• impaired cell migration
• impaired connective tissue deposition
Degrades Growth Factors
TNFα and IL-1β

↑ Production MMPs and ↓ TIMPs

Biochemical Differences

Healing Wounds Chronic Wounds

• cell mitosis • mitogenic activity
• pro-inflammatory • pro-inflammatory
cytokines cytokines
• MMPs • MMPs
• Growth factors • Varied # growth
• Cells capable of factors
responding to • Senescent cells
healing signals
Clinical Assessment

• Does this patient have the ability to

heal?
• Consider overall goals of care
• Address wound etiology
• Consider factor that contribute to
impaired wound healing
Wound Etiology

Mechanical
Arterial
Venous Address the
Neuropathic etiology
Malignancy
Vasculitic
Other
Assessment
Systemic Factors

Age Medications

Body Build Tissue

Oxygenation
Stress
Concomitant
Disease
Nutrition
Assessment

Local Factors
Perfusion

Mechanical Necrotic tissue

stressors

Edema Bacterial Burden

Wound
temperature Desiccation

Cytotoxic agents Excess exudate

Wound Bed Preparation - Defined

Wound bed preparation is the

management of a wound in order to
accelerate endogenous healing or to
facilitate the effectiveness of other
therapeutic measures

1Falanga, 2003
International Advisory Panel on
Wound Bed Preparation
Gregory Schultz, PhD Keith Harding, MD
Vincent Falanga, MD Marco Romanelli, MD
Gary Sibbald, MD Michael Stacey, DS
Elizabeth Ayello, PhD Luc Teot, MD, PhD
Caroline Dowsett Wolfgang Vanscheidt, MD

Wound Bed Preparation:

A Systematic Approach to Wound Management
Wound Repair and Regeneration, 2003; 11:1-28
20Schultz, Sibbald, Falanga, et al, 2003
TIME Principles of Wound Bed Preparation
Tissue non Infection or Moisture Edge of Wound
viable or inflammation imbalance non advancing or
deficient undermined
Defective matrix High bacterial Non-migrating
Desiccation keratinocytes
and cell debris counts or
or excess Non-responsive
prolonged
fluid wound cells
inflammation

Dressings Biological Agents

Debridement Antimicrobials
Compression Adjunct Therapies
Debridement

Restore Low bacterial Restore cell

Stimulate
wound base counts and migration,
keratinocyte
and ECM controlled maceration
migration
proteins inflammation avoided
T
Tissue:
Non-viable or
Deficient
Debridement

Why debride?
• Enhance wound assessment
• Decrease potential for
infection
• Necrotic tissue delays
formation of granulation and
epithelial tissue
Debridement

What to debride?
• Slough - moist yellow, tan or
gray non-viable tissue.
• Eschar - dry, leathery
Debridement Methods

Surgical
Mechanical
Autolytic
Enzymatic
Biological

Select the most appropriate method for

the patient’s condition and goals of care
Surgical Debridement

• Scalpel
• Scissors
• Curet
• Laser

Recommended for removal of thick, adherent

eschar and devitalized tissue in large wounds
Surgical Debridement
Considerations
• The most aggressive debridement
• Requires adequate perfusion
• Tissue or bone cultures
• Not recommended for severely compromised
patients
• Analgesia/anesthesia required
• Licensure/Skill
• Associated with increased healing rates
among patients with diabetic foot ulcers5
5Steed et al, 1996
Surgical Debridement

Courtesy David Armstrong, MD

 Mechanical Debridement

Definition - The removal of foreign

material and dead or damaged
tissue by the use of physical
forces.

Methods
– Irrigation
– Wet-to-dry dressings
– Hydrotherapy
Mechanical Debridement

Considerations
• Aggressive debridement
• Wet-to-dry dressing may be painful
• Trauma to capillaries can cause bleeding
• Skin maceration may occur
• Dressing changes may be time-consuming
Mechanical Debridement

A B
Autolytic Debridement

Definition - The process by which the wound

bed utilizes phagocytic cells and proteolytic
enzymes to remove debris.

This process can be

promoted and enhanced by
maintaining a moist wound
environment.
Autolytic Debridement

Considerations
• Less aggressive debridement
• Slower than other methods
• Easy to perform
• Little or no discomfort
• Performed in any setting
• Contraindicated in the presence of infection
Autolytic Debridement
Enzymatic Debridement

Definition - The use of topically applied chemical

agents to stimulate the breakdown of necrotic
tissue.

Common Topical Agents

– Papain-Urea
– Papain-Urea - Chlorophyllin
– Collagenase
Enzymatic Debridement

Collagenase
• Derived from Clostridium Hystoliticum
• Highly specific for peptide sequence found in
collagen
• Less aggressive debridement
• Site of action – collagen fibers anchoring
necrotic tissue to the wound bed

10Harper (1972) 11Boxer (1969) 12Varma (1973)

Enzymatic Debridement

Papain-Urea
• Proteolytic enzyme derived papaya6
• Urea is added as a denaturant6
• Site of action – cysteine residues on protein8
• Inactive against collagen6
• Aggressive debridement

6Falabella (1998) 8 Sherry and Fletcher (1962

Papain-Urea Mode of Action
Enzymatic Debridement

Papain-Urea Chlorophyllin
• Contains Papain, Urea and Sodium Copper
Chlorophyllin
• Sodium copper chlorophyllin is a chlorophyll
derivative
– Anti-agglutinin
• Results in anti-Inflammatory action
– Reduces odor

7Morrison J, Casali J (1957)

Enzymatic Debridement
Considerations
• Should be painless
• Less traumatic than surgical or mechanical
debridement
• Easy dressing change
• Observe caution with infected wounds
• Consider the use of enzymatic debridement
for individuals who:
– Cannot tolerate surgery
– Reside in a long-term-care facility
– Receive care at home*

*Agency for Healthcare Research and Quality (1994)

Enzymatic Debridement

Eschar Preparation
• Cross Hatching
• Hydrating agents
Debridement Methods

More Aggressive Less Aggressive

• Surgical • Autolytic
• Mechanical • Collagenase
• Papain-Urea • Papain-Urea
Chlorophyllin
Debridement Decisions:
Clinical Indications
Aggressive Methods
• Majority of wound
covered with necrotic
tissue
• Goal of therapy is quick
removal of necrotic tissue
• Wound continues to
improve with current
therapy
Debridement Decisions:
Clinical Indications

Less Aggressive Methods

• Majority of wound is
clean and granulating
• No threat to patient’s
health
Debridement Decisions

Selecting the Appropriate Method

• Wound characteristics
• Degree of desired aggressiveness
• Time available for debridement
• Skill/licensure of clinician
• Care setting

Clinicians may choose more than one method of

debridement – e.g., surgical, followed by enzymatic
Most Aggressive - Surgical
Aggressive
Less Aggressive

The right method is a clinical decision that requires judgment

I
Infection or
Inflammation
Risk Factors that Increase the Risk for
Infection
Systemic Local
• Vascular disease • Large wound area
• Edema • Increased wound depth
• Degree of chronicity
• Malnutrition
• Anatomic location (distal
• Diabetes mellitus extremity, perineal)
• Alcoholism • Presence of foreign bodies
• Prior surgery or radiation • Necrotic tissue
• Drugs e.g. • Mechanism of injury
corticosteroids Degree of post-wounding
contamination
• Inherited immune
defects • Reduced perfusion
 Bacterial Burden
Contamination - Infection Continuum

N
O
TI
N

ZE Y
O

C
NI LL
D
TI

FE
D

LO ICA
ZE
A

IN
IN

NI

CO IT
AM

LO

CR
NT

CO
CO

Local Systemic
Bacterial Burden
Why is an increased Bacterial Burden
Problematic?
• ↑ metabolic load
• Produces endotoxins and proteases
• Stimulates a pro-inflammatory wound
environment
• Wounds don’t heal
 Host Bacterial quantity
and
Resistance virulence

Bacterial
Balance

Local perfusion Adhesins

Immunosuppression Cell Capsules
Diabetes Biofilms
Medications Antibiotic Resistance

3Sibbald et al (2000) 14Dow (2001)

Clinical Presentation
“Classic” Signs & Symptoms of Infection

Advancing erythema
Acute Wound Infection
Fever
or
Warmth
Severe
Edema / swelling
Chronic Wound
Pain
Infection
Purulence
Clinical Presentation
Secondary Signs & Symptoms of Infection
Delayed healing
Critically Colonized
Change in color of wound
- bed
↑ Bacterial Burden Friable granulation tissue
- Absent or abnormal
Local granulation tissue
Wound Infection ↑ or abnormal odor
↑ serous drainage
↑ pain at wound site
15Cutting & Harding (1994)
16Gardner, Frantz & Doebbeling (2001)
Reducing Bacterial Burden

Interventions
• Debridement
• Wound cleansing
• Avoid routine use of antiseptics
– Betadine
– Hydrogen Peroxide
– Acetic Acid
– Dakin’s Solution
Recommendations for Wound Bed Prep

N
O

ED
TI
A

Z
IN

NI
AM

LO
NT

CO
CO

Wound progressing

•Routine wound cleansing

•Exudate management
•No indication for cultures
Recommendations for Wound Bed Prep

lly l
ca d a
ir ti nize Loc tion
C lo ec
o nf
C I

Delayed healing

• Thorough cleansing • Debridement if needed

• Exudate management • Consider topical antimicrobials
-Silver dressing
-Cadexomer idodine gel
Topical Antimicrobials - Silver

• Centuries of proven antimicrobial activity

• Cytotoxicity concerns associated with
carriers not silver - ex. Silver nitrate, Silver
sulfadiazine
• Traditional delivery required repeated
applications due to binding with chlorine and
proteins
• New silver dressings allow for continued
silver release - up to 7 days
17Demling and DeSanti (2001)
Nanocrystalline Silver

• Decreased size of silver

particles leads to increased
proportion of surface atoms
compared with internal Magnification of
atoms15 normal silver

• It is believed that the

nanocrystalline structure
is responsible for the rapid
and long lasting action15 Magnification of
Nanocrystalline Silver
17Demling
(<1 micron)
and DeSanti (2001)
Case Study

Day 0 Day 20
10 year old venous leg ulcers After treatment with
previously treated with nanocrystalline silver
compression and SSD
18Data on file
Topical Antimicrobials
Cadexomer Iodine
• Iodine is a well known antimicrobial agent
• 0.9% iodine is carried in polysaccharide
beads
• Provides a slow sustained release of
iodine in non-cytotoxic concentrations
• High rate of absorption from exudating
ulcers.
• No documented cases of bacterial
resistance.
Recommendations for Wound Bed Prep

N
ni y
e

d
lo all
d
at

IO
ze
ze

Co itic
in

CT
ni
m

Cr
lo
a

FE
nt

Co
Co

IN
Impaired healing

• Thorough cleansing Courtesy AAWC

• Debridement if needed
• Exudate management
• Consider topical antimicrobials
•Silver dressing
•Cadexomer iodine gel

• Systemic antibiotics
Moisture Imbalance - Dry

• Desiccation slows epithelial migration

• Painful and uncomfortable for the
patient
• Delays normal healing process
• Acts as a source of infection
• Longer treatment time
• Increased cost
Moisture Imbalance - Wet

• Maceration of
peri-wound skin
• Chronic wound
fluid issues
Exudate Management

Chronic Wound Fluid

Bacterial Breakdown of
Burden Necrotic tissue Edema
(Debridement)

Microbial
Compression
Management
Dressing
Selection
Chronic Wound Fluid - Edema

Ankle-Brachial Index & Compression

< 0.5 --- 0.6 ------------- 0.8 ---------------1.0

High
Reduced
None
Dressing Selection Factors

• Amount of exudate
• Anatomical location
• Presence of dead space (Depth,
undermining, tunneling)
• Condition of surrounding skin
• Caregiver ability
• Healable vs. non-healable wound
• Cost
Managing Moisture Imbalance
Exudate Amount
None Small Moderate Large

Films
Hydrogel
Hydrocolloid
Alginate
Foams
Specialty Absorbent
Small Amount of Exudate

B Courtesy AAWC
A

C
D
Moderate Amount of Exudate

A B

D
C
Large Amount of Exudate

A B
E
Edge of Wound
Non-advancing or
Undermined
Edge of Wound
Non-advancing or Undermined
Problem
• Cells not capable of responding to healing
signals
• Hyper-proliferation of epidermal cells
occurs at the wound margins
• Epidermis fails to migrate across the
wound
Edge of Wound
Non-advancing or undermined

Interventions
• Debridement
• Biological Agents
• Skin Grafts
• Adjunctive Therapies

20Adapted from Schultz, Sibbald, Falanga, et al, 2003

Continuous Assessment

Systemic
Etiology Factors
Patient
Local Time
Factors Principles
References
1 Falanga V. (Ed.). New Concepts in Wound Bed Preparation. Springer-Verlag GmbH & Co. KG, Science
Communication Corporate Publishing, Berlin Heidelberg, 2003.
2 Falanga V. Classifications for wound bed preparation and stimulation of chronic wounds. Wound Repair and
Regeneration 2000;8:347-352.
3 Sibbald RG, Williamson D, Orsted HL, Campbell K, Keast D, Krasner D, Sibbald D. Preparing the Wound Bed -
Debridement, Bacterial Balance and Moisture Balance. O/WM 2000;46(11)14-35.
4 Mast BA, Schultz GS. Interactions of cytokines, growth factors, and proteases in acute and chronic wounds. Wound
Repair and Regeneration 1996;4:411-420.
5 Steed DL, Donohoe D, Webster MW, Lindsley l, and the Diabetic Ulcer study Group. Effect of Extensive Debridement
and Treatment on the Healing Diabetic Foot Ulcer. Journal of the American College of Surgeons 1996;183:61-64.
6 Falabella A. Debridement of Wounds. Wounds 1998:10;1C-9C.
7 Morrison J, Casali J. Continuous Proteoplytic Therapy for Decubitus Ulcers. Am Journal of Surgery 1957; 93: 446-448.
8 Sherry S. and Fletcher AP. Proteolytic enzymes: a Therapeutic evaluation. Clinical Pharmacology and Therapeutics
196X;1:202-226.
9 Lutterman A, Curtis R, Blache C, Johnston K & Frye K. Accuzyme Papain/Urea Ointment vs. Collagenase Santyl
Ointment in the Treatment of Partial Thickness Burn Wounds, presented at SAWC, 2001
10 Harper E. Studies on the Mechanism of Action of Bacterial Collagenase. in Collagenase. Mandl, I., ed., Gordon&
Breach, Science Publishers, Inc. New York, 1972.
11 Boxer AM, Gottesman N, Bernstein H, Mandl I. Debridement of Dermal Ulcers and decubiti with collagenase.
Geriatrics 1969;24(7):75-86.
References
12 Varma AO, Bugatch E, German FM. Debridement of Dermal Ulcers with Collagenase. Gynecology & Obstetrics
1973;136:281-281.
13 Robson, MC. Wound Infection: A Failure of Wound Healing Caused by an Imbalance of Bacteria. Surgical Clinics of North
America 1997;77(3)637-651.
14 Dow G. Infection in chronic wounds. In: Krasner DL, Rodheaver GT, Sibbald RG (eds). Chronic Wound Care: A Clinical
Source Book for Healthcare Professsionals, Third Edition. Wayne, PA: HMP Comunications, 2001:343-356.
15 Cutting KF, Harding KG. Criteria for Identifying wound infection. Journal of Wound Care 1994;3(4):198-201.
16 Gardner SE, Frantz RA, Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized wound
infection. Wound Repair and Regeneration 2001;9(3):178-186.
17 Demling R. DeSanti L. Effects of Silver on wound Management. Wounds 2001;13(1) Supplement A:4-15.
18 Data on file
19 Schultz G, Mast B. Molecular Analysis of the Environment of Healing and Chronic Wounds: Cytokines, Proteases and Growth
Factors. Wounds 1998;10:1F-9F
20 Schultz G. sibbald RG, Falanga V, Ayello A, Dowsett C, Harding K, Romanelli M, Stacey M, Teot L, Vanscheidt W. (2003)
Woud bed preparation: a systematic approach to wound management. Wound Repair & Regeneration 11(1): 1-28.
21 Enoch S, Harding K. (2003). Wound bed preparation: the science behind the removal of barriers to healing. Wounds, 15(7):
213-229.
22 Sibbald RG. Topical Antimicrobials. Ostomy/Wound Management 2003;49(5A-suppl): 3-33.
23. Kane DP, Krasner D. In: Chronic Wound Care. 2nd ed. Health Management Publications Inc; 1997:1-4.