Transcript No Slide Title

Principles of Wound
Healing
WHAT IS A WOUND?
Wound(woond): Break in
the continuity of soft or
hard parts of the body
structures caused by
violence or trauma to
tissues.
Common chronic wounds of the skin and
soft tissues
Arterial
Venous
Pressure
Diabetes
Collagen Vascular disease
Udder
Chronic Versus Acute Wounds
Normal acute wounds caused by surgery or
trauma usually heal and close rapidly
A chronic non-healing wound has been defined as
a wound that fails to proceed through the orderly
and timely series of events required to produce a
durable structural, functional, and cosmetically
acceptable closure.
Reference: Lazarus GS, Cooper DM, Knighton DR et al. Definitions and Guidelines for Assessment of Wounds and Evaluation
of Healing. Arch Dermatol. 1994;130:489-493.
Acute Wounds
• Cells are viable, able to respond to
growth stimuli
• Sufficient growth factors are
released in the wound environment
• Cells proliferate and can migrate
and synthesize components of new
tissue
Reference: Monaco JL, Lawrence TL. Acute wound healing; an overview. Clinics in Plastic Surgery 30 (2003): 1-
12.
Chronic Wounds
• Growth factors may be deficient
• Increased Bacteria
• Decreased oxygen
• Cells are senescent, unable to respond to
growth factors
• Cells may be slow to proliferate and migrate
(< 0.5 mm/week wound closure rate)
References:
Stanley A, Osler T. Senescence and the healing rates of venous ulcers. J Vasc Surg 2001 Jun;33(6):1206-11
Mulder GD, Vande Berg JS. Cellular senescence and matrix metalloproteinase activity in chronic wounds. Journal of the
American Podiatirc Medical Association. Jan 2002 92(1):34-37.
Biological and Chemical Defects
in Chronic Wounds
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Deficient growth factors
Diminished granulation tissue
Delayed epithelialization
Defective extracellular matrix formation
Excessive proteases (MMPs)
Reference: Nwomeh BC, Yager DR, Cohen,IKC. Physiology of the chronic wound. Clinics in Plastic Surgery July 1998
25(3):341-356.
Growth factor deficiencies
found
in chronic wounds include:
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Platelet Derived Growth Factor (PDGF)
Transforming Growth Factor Beta (TGFß)
Vascular Endothelial Growth Factor (VEGF)
Insulin-like Growth Factor (IGF-1)
Keratinocyte Growth Factor (KGF)
Reference: Robson MC, Smith PD. Topical use of growth factors to enhance healing. In Cutaneous Wound Healing editor V.
Falanga Martin Dunitz, London 2001 pp379-398.
Good Wound Care:
Clinical practices which support
the normal healing process
Key Considerations – Good Wound
Care
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Infection control
Sharp Debridement
Moist wound environment
Off-loading/compression therapy
Nutritional status
Sharp Debridement
Removes:
• Devitalized tissues
• Bacteria and
proteolytic enzymes
• Senescent cells
Know the wound
etiology!
Venous stasis etiology
Arterial etiology
Neuropathic (Diabetic)
Etiology
Pressure etiology
Collagen vascular
etiology
Hypercoagulopathy
Phases of Normal Wound Healing
• Hemostasis
• Inflammation
• Proliferation
• Remodeling
Hemostasis
• Immediate reaction of small vessels
in the area of injury is
vasoconstriction
• Release of platelet cytokines (growth
factors)
Inflammatory Phase
• Usually lasts from time of injury
through 3 days
• Polymorphonuclear leukocytes
(PMN’s) are the first white blood cells
to enter the wound
• Peak in 24-48 hours
• Macrophages appear at 48-96 hours
Proliferative Phase
• Fibroblasts appear in the wound on day 3,
peaking on day 7
• Granulation tissue forms consisting of
fibroblasts, inflammatory cells and
capillaries in an extracellular matrix of
collagen, fibronectin and glycosaminoglycans
(GAGs)
• Fibroblasts are attracted to the wound and
stimulated to proliferate by cytokines
(growth factors) produced by platelets,
macrophages and lymphocytes
Proliferative Phase
• Fibroblasts lay down the extracelluar
matrix (collagen)
• Endothelial cells migrate in response
to angiogenic stimuli and form new
capillaries
• Epithelial cells migrate and begin the
process of reepithelialization
Remodeling Phase
• Usually starts from month 3 and can
last up to a year or more
• Reorganization of collagen
• Increase in tensile strength
Why won’t this wound heal?
Why won’t this wound heal?
Why won’t this wound heal?
Factors Affecting Normal Wound Healing
• Poor arterial circulation
• Infection
• Venous hypertension
• Diabetes
• Steroid usage
• Continued pressure
• Poor nutrition
• Cytotoxic substances
• Malignancies
Factors Affecting Normal Wound Healing
• Foreign bodies
• Cigarette smoking
• Radiation
• Alcoholism
• Aging
•Compliance
Poor Arterial Circulation
• inadequate supply of oxygen and nutrients
required for healing
• Hypoxia impairs neutrophil function
• decreases collagen synthesis and cross linking
• decrease in tensile strength
• increases susceptibility to infection
Infection
• 100,000 bacteria/gram of tissue or greater and
the body cannot control without intervention
• Beta hemolytic Strep is an exception. Wound
healing is affected no matter what the
concentration
• Bacteria secrete proteases, hemolysins and
inhibitors of leukocyte chemotaxis
Infection
Venous hypertension
• superficial venous insufficiency
• incompetent perforator vein with normal
deep vein
• venous hypertension:capillary distention,
leakage of fibrinogen from the blood to
dermis. Prevents oxygen diffusion nutrient
transport, chronic leg edema
• periwound inflammation
• compression is the cornerstone of treatment
• color duplex Doppler's are the gold standard
for diagnosis
Venous Stasis
Diabetes
• Peripheral neuropathy with sensory impairment
• Motor neuropathy leading to foot deformity
• Autonomic neuropathy (decreased sweating and
suppleness of the skin)
• Peripheral vascular disease (atherosclerosis)
• Immunodeficiency
• Poor glucose control
• Denial of the disease
• Charcot arthropathy
CHARCOT
ARTHROPATHY
Glucocorticoid Usage
• Prednisone use: Increased risk of infection
• Use of steroids can increase wound
complications 2-5 times
• Suppression of inflammation
• Decreased wound strength
• Inhibition of wound contracture
• Delayed epithelialization
• Topical vitamin A enhance epithelialization
• Oral vitamin A can increase collagen
deposition
Continued Pressure
• Pressure, friction, shear
•Tissue hypoxia
• Tissue death
• Inhibition of normal wound healing
mechanism to proceed
• Muscle can degenerate with as little as 60
mm Hg
• Pressure over some bony prominences can
reach 2600 mm Hg
Cytotoxic Substances
• Topical products such as hydrogen peroxide,
vinegar, povidone-iodine (Betadine), Gentian
Violet solution, Phisohex, Dakins solution.
• OK to use for a couple of days if your goal is
to reduce bacterial count. SHOULD NOT be
used on wounds once they are clean and in the
healing phase.
Malignancies
• Wounds that do not fit the profile of a
typical chronic wound or is not progressing
in the time frame that one might expect
• Squamous cell carcinoma, basal cell
carcinoma, sarcomas, malignant
melanomas, leukemias
Foreign Bodies
• Nidus for infection: Hematomas,
Dysvascularized bone, tendon, cartilage,
metal objects, glass, wood, thorns
Smoking
• Limits functional tissue perfusion
• Cutaneous vasoconstriction and decreased
wound contraction as a direct effect of nicotine
Radiation
• Thinning of the epidermis
• Decrease in quantity of blood vessels
• Increase fibrosis in dermis
• Fibroblasts permanently damaged
• Irradiated site becomes relatively ischemic
• Radiation damaged skin is easily damaged
• Poor inflammatory response after injury
• Poor angiogenesis
Osteoradionecrosis
Alcoholism
• Chronic alcohol usage can cause slow cellular
growth and slower collagen accumulation
Aging
• Affects every stage of healing
• Decrease in wound tensile strength, delayed
epithelialization, more tissue breakdown than
synthesis
Calciphylaxis
Pyoderma gangrenosum
Be aware!
Compliance
Current Wound Healing Concepts
• Determine the wound etiology
• Take wound biopsies
• Ensure adequate perfusion
• Treat infection (take tissue cultures not swab
cultures)
• Remove pressure from the wound
• Aggressive frequent debridements
• Keep wounds moist
•Compression is the key to venous stasis ulcers