Download Advances-in-Wound-care-2007 - Rex Moulton

Advances In Wound Care
2007
Rex Moulton-Barrett,MD
Wound aspects
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Etiology
Types: Acute/Chronic
Patho-physiology
Treatment:Pain
Ulceration
Edema
Exudate
Components of Normal Wound Healing
•Coagulation
process
•Inflammatory
process
A) Immediate to 2-5 days
B) Hemostasis : Vasoconstriction , Platelet
aggregation , Thromboplastin clot
C) Inflammation: Vasodilation , Phagocytosis
•Migratory/
A) 2 days to 3 weeks
B) Granulation: Fibroblasts lay collagen, Fills & new capillaries
C) Contraction: Wound edges pull together to reduce defect
D) Epithelialization: Crosses moist surface up to 3 cm
•Remodeling
A) 3 weeks to 2 years
B) New collagen forms which increases tensile strength
C) Scar tissue is only 80 percent as strong as original tissue
Proliferative
process
process
Injury: hours / days
weeks
Biochemical Differences
Healing wounds
• cell mitosis
• pro-inflammatory
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•
•
cytokines
Matrix metalloproteinases
Growth factors
Cells capable of
responding to
healing signals
Chronic wounds
• mitogenic activity
• pro-inflammatory
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•
•
cytokines
MMPs
Varied # growth
factors
Senescent cells
Wound Etiology
Mechanical
Arterial
Venous
Neuropathic
Malignancy
Vasculitic
Metabolic
Address the etiology
Types of Ulcers & Pathophysiology
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Diabetic: pressure(joint/bone)>neuropathic>ischemic>infective
Venous Stasis: intercellular pressure>ischemia ( post-capillary )
Arterial: ischemia ( pre-capillary )
Pressure/Decubitus Sore: neuropathic>boney/joint pressure
soft tissue infection is a secondary acute or chronic event
joint infection and or osteomyelitis chronic
secondary amyloidosis chronic
Marjolin Ulcer: squamous cell carcinoma or sarcoma >3 yrs
Pressure Sore Staging
National Pressure Ulcer Advisory Panel (NPUAP)
•
Stage 1
skin,
Nonblanchable erythema intact skin,
discoloration of the skin, warmth, edema, induration, or hardnes
ulcer defined area of persistent redness in lightly pigmented
in darker skin tones, persistent red, blue, or purple hues.
•
Stage 2
Partial thickness skin loss involving epidermis, dermis, or both.
ulcer is superficial with abrasion, blister, or shallow crater.
•
Stage 3
Full thickness skin loss subcutaneous tissue that
may extend to, but not through, underlying fascia.
ulcer may have deep crater or undermining adjacent tissue.
•
Stage 4
Full thickness skin loss with, tissue necrosis, muscle, bone, or
supporting structures (e.g., tendon, joint capsule)
Undermining and sinus tracts
Diabetic Foot Ulcer
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DM: 10 Million USA today
Immunopathy, vasculopathy, neuropathy,erythrocyte hemopathy
Misconception: small vessel disease
Multidisciplinary approach: podiatry, vascular, plastics, physical therapy
Neuropathy primary problem: small muscle contractures ( intrinsic minus )
Secondary ligament and tendon glycosation leads to shortening
Secondary joint contracture: asensate pressure sore
Treatment: restore balance and distribute load and protect surfaces
Examples: midfoot ulcer: remove underlying metaphysis (118,000 lb/sq”)
heel ulcer: Tendo achilles Z lengthening to 90 degrees
Cuboid dislocation and Charcot Foot: requires internal fixation
Venous Stasis Ulcer
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Cause: intercellular & post-capillary stasis and edema
Secondary causes: infection, dry wound, shearing forces
Classic management: Zinc and compression Una Boot
Rule out concomitant arterial ischemia
Modern Work-up and treatment:
– Duplex u/s and cultures
– If significant venous reflux disease: end-venous ablation and venectomy
– Local treatment is a 4 component weekly:
silver dressing
3 layer compression
With or without absorbent dressing
Venous Stasis Ulcers & Compression
• Circ-aid ( R:Allegra Medical ): Nonelastic, latex-free,
40 mmHg compression therapy system
Uses interlocking Velcro® bands
Washable and reusable
• Circ-aid vrs Una Boot: 45% faster , 38% cheaper than Una Boot
• Cir-aid: less surface shear and focal compression than 30mmHg stockings
at 2 months 1/2 the edema remains a.c.t. similar stockings
67% of pts. With failed Una and stockings healed at 12 months
Ischemic and Post - Radiation Ulcers
• Multidisciplinary approach
• Work-up arteriograms and duplex u/s
digital toe pressures
• Primary treatment: revascularize arterial
• Secondary infections, osteomyelitis benefit
from hyperbaric oxygen providing arterial
supply adequate, ie toe pressures helpful
Assessment – Systemic Factors
• Age
• Medications
• Body build
•
• Stress
• Tissue
• Nutrition
oxygenation
• Concomitant
disease
Assessment – Local Factors
• Perfusion
• Mechanical
• Necrotic tissue
• Edema
• Bacterial burden
• Wound
• Desiccation
stressors
temperature
• Cytotoxic
agents
• Excess exudate
TIME Principles of Wound Bed Preparation
Wound bed preparation accelerates healing
Edge of wound
Tissue non
Infection or
viable or
deficient
inflammation
Defective
matrix and cell
debris
High bacterial
counts or
prolonged
inflammation
Desiccation
or excess
fluid
Non-migrating
keratinocytes
Non-responsive
wound cells
Debridement
Antimicrobials
Dressings
compression
Biological agents
Adjunct Therapies
Debridement
Restore wound
base and ECM
proteins
Low bacterial
counts and
controlled
inflammation
Restore cell
migration,
maceration
avoided
Stimulate
keratinocyte
migration
Moisture
imbalance
non advancing
or undermined
Suction Vac
• 0.15 mm pore, 125 mmHg suction:
• Increased angiogenesis, VEGF, nitric oxide?
• Increased vessels,granulation: up to 5x’s
• Decreased exudate, hypoxia
• Dressing changes/2 days, but costly rental
76 in Jan 2005
KCI: Education
• http://www.kci1.com/education/index.asp
• See whp1.swf
T
Tissue
Debridement
Why debride ?
What to debride ?
• Enhanced wound assessment
• Slough-moist yellow, tan
• Decrease infection potential/extent
or gray non-viable tissue
• Increase granulation epithelialization • Eschar-dry, leathery
Debridement Methods
• Surgical:
excise
• Mechanical: adherance,sheer, irrigate
• Autolytic: topical
• Enzymatic: topical
• Biological: topical
Surgical Debridement
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Scalpel
Scissors
Curet
Laser
Hydro-Scapel
U/S Hydro
Recommended for removal of thick,
adherent eschar and devitalized
tissue in large wounds
Mechanical Debridement
Definition - The removal of foreign
material and dead or damaged tissue
by the use of physical forces.
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Methods
Irrigation
Wet-to-dry dressings
Hydrotherapy: Whirlpool
Suction Vac
Mechanical Debridement Considerations
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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
Autolytic Debridement
•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
•Contraindication: infection
Autolytic Debridement
Enzymatic Debridement
•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
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Papain-Urea
Proteolytic enzyme derived papaya6
Urea is added as a denaturant6
Site of action – cysteine residues on protein8
Inactive against collagen6
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
– long-term-care facility
– home care*
*Agency for Healthcare Research and Quality (1994)
Autolytic,
Collagenase,
Papain-Urea-Chlorophyllin
The right method is a clinical decision that requires judgment
I
Infection or inflammation
Bacterial Balance
• Control mechanism
• Intact skin is a physical barrier
• pH is not conducive to bacterial growth
• Skin secretes fatty acids and antibacterial
•
polypeptides
Normal flora prevent pathogenic flora
from establishing
Risk Factors for Infection
Systemic
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Vascular disease
Edema
Malnutrition
Diabetes mellitus
Alcoholism
Prior surgery or radiation
Drugs e.g. corticosteroids
Inherited immune defects
Local
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Large wound area
Increased wound depth
Degree of chronicity
Anatomic location (distal
extremity, perineal)
• Presence of foreign bodies
• Necrotic tissue
• Mechanism of injury
• Degree of contamination
• Reduced perfusion
Bacterial Burden
Contamination - Infection continuum
Bacterial Burden
• Tissue bacterial levels > 105 have
consistently resulted in impaired healing
causing:
• Metabolic load
• Produces endotoxins and proteases
13Robson
(1997)
14Dow
(2001)
Bacterial quantity
and virulence
Host resistance
Bacterial balance
Adhesins
cell capsules
biofilms
Antibiotic resistance
Local perfusion
immunosuppression
Diabetes
medications
3Sibbald
et al (2000)
12Dow
(2001)
3 Rules for Topical Antimicrobial Agents
•Do not use antibiotics that are used systemically – ability to
breed resistant organisms (topical gentamiycin, tobramycin)
•Do not use agents that are common allergens (neomycin,
gentamycin, amikacin, tobramycin, bacitracin, lanolin)
•Do not use agents that have high cellular toxicity in healable
wounds (povidone iodine, chlorhexidine, hydrogen peroxide)
22Sibbald
2003
Topical Antimicrobials: Silver
• Centuries of use
• Cytotoxicity 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 in to the dressing - up to 7 days
17Demling
and DeSanti (2001)
Why Silver for Wound Bed Preparation?
• Broad spectrum antimicrobial: yeasts, molds &
bacteria, including MRSA
• Kills microbes on contact:
inhibitiion cellular respiration
denatures nucleic acids
alters cell membrane permeability
• Does not induce resistance:
if used at adequate levels
• Low mammalian cell toxicity
• Anti-inflammatory activity:
delivery system dependent)
Nanocrystalline Silver
• Decreased size of silver particles
leads to increased proportion of
surface atoms compared with
internal atoms15
Magnification of normal Silver
\
• It is believed that the
nanocrystalline structure is
responsible for the rapid and long
lasting action15
Magnification of Nanocrystalline Silver (< 1 micron)
17Demling
and DeSanti (2001)
Evaluating Silver Products
• Minimum bactericidal concentration
(MBC) - amount of antimicrobial agent
required to kill a given microbe
MBC is represented by a log reduction of 3
Stratton et al (1991)
– The silver required varies from 5ppm - 50+
ppm for clinically relevant microbes
Yin et al (1999) & Hall (1987)
– MBC of silver for MRSA = 60.5 ppm
Calculated from Maple et al (1992)
Case Study
• Day 3650
• Day 20
• 10 year old venous leg ulcers
• Treated: silver nanocrystal therapy
• previously treated: compression and SSD
Topical Antimicrobials Cadexomer Iodine
• Iodine is a well known antimicrobial agent
• 0.9% iodine is carried in polysaccharide beads
• Provides sustained release iodine:non- cytotoxic concentration
• High rate of absorption from exudating ulcers
• No documented cases of bacterial resistance
Recommendations for Wound Bed Prep
Impaired healing
• Thorough cleansing
• Debridement if needed
• Exudate management
– Consider topical antimicrobials
– Silver Cadexomer iodine gel dressing
• Systemic antibiotics
M
moisture
Exudate Management
1960’s: Moist Wound Environment Dr. George Winter
– Improved Collagen synthesis & granulation tissue
– Faster Cell migration and epithelial resurfacing
– Prevention of scabs, crusts, and eschar
Moist Wound Environment
•Additional benefits
• Faster healing
• Capacity for autolysis
• Decreased rates of infection
• Reduced wound trauma
• Decreased pain
• Fewer dressing changes
• Cost effective
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 from a Chronic Wound
• Different from acute wound
• Imbalance of growth factors and
pro-inflammatory cytokines
• Excessively high levels of proteases
• Degrades ECM and selectively inhibits proliferating cells
21Enoch
and Harding, 2003
Exudate Management
Chronic wound
fluid
Edema
Breakdown of
Bacterial
Necrotic tissue
burden
Microbial (debridement)
Compression
management
Dressing
selection
Chronic Wound Fluid - Edema
•Ankle-Brachial index & compression
< 0.5 --- 0.6 ------------- 0.8 ---------------1.0
High
None
Reduced
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
Small Amount of Exudate
A
B
C
D
Moderate Amount of Exudate
Large Amount of Exudate
A
B
Managing Moisture Imbalance
• Exudate amount
None
• Films
• Hydrogel
• Hydrocolloid
• Alginate
• Foams
• Specialty Absorbent
• Suction Vac
Small
Moderate
Large
E
Edge of Wound Non-advancing or Undermined
• 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
Useful teaching resources
• Wound Care Information Network
http://www.medicaledu.com/default.html
• KCI
http://www.kci1.com/products/vac/vac/index.asp
• Smith & Nephew
http://wound.smith-nephew.com/us/Home.asp