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Principles of Wound Healing

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Title: Principles of Wound Healing


1
Principles of Wound Healing
2
WHAT IS A WOUND?
3
Wound(woond) Break in the continuity of soft or
hard parts of the body structures caused by
violence or trauma to tissues.
4
Common chronic wounds of the skin and soft
tissues Arterial Venous Pressure Diabetes Collagen
Vascular disease Udder
5
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.
1994130489-493.
6
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.
7
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 (lt
    0.5 mm/week wound closure rate)

References Stanley A, Osler T. Senescence and
the healing rates of venous ulcers. J Vasc Surg
2001 Jun33(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.
8
Biological and Chemical Defects in Chronic Wounds
  • 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.

9
Growth factor deficiencies found in chronic
wounds include
  • 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.

10
Good Wound CareClinical practices which
support the normal healing process
11
Key Considerations Good Wound Care
  • Infection control
  • Sharp Debridement
  • Moist wound environment
  • Off-loading/compression therapy
  • Nutritional status

12
Sharp Debridement
  • Removes
  • Devitalized tissues
  • Bacteria and proteolytic enzymes
  • Senescent cells

13
Sharp Debridement Improves Incidence of Complete
Healing with Becaplermin
Adapted from Steed DL. et. al. J Am Coll Surg
199618361-64.
14
Know the wound etiology!
15
Venous stasis etiology
16
Arterial etiology
HIPAA
17
Neuropathic (Diabetic) Etiology
18
Pressure etiology
19
Collagen vascular etiology
20
Hypercoagulopathy
21
  • Phases of Normal Wound Healing
  • Hemostasis
  • Inflammation
  • Proliferation
  • Remodeling

22
  • Hemostasis
  • Immediate reaction of small vessels in the area
    of injury is vasoconstriction
  • Release of platelet cytokines (growth factors)

23
  • Inflammatory Phase
  • Usually lasts from time of injury through 3 days
  • Polymorphonuclear leukocytes (PMNs) are the
    first white blood cells to enter the wound
  • Peak in 24-48 hours
  • Macrophages appear at 48-96 hours

24
  • 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

25
  • 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

26
  • Remodeling Phase
  • Usually starts from month 3 and can last up to
    a year or more
  • Reorganization of collagen
  • Increase in tensile strength

27
Why wont this wound heal?
28
Why wont this wound heal?
29
Why wont this wound heal?
30
  • Factors Affecting Normal Wound Healing
  • Poor arterial circulation
  • Infection
  • Venous hypertension
  • Diabetes
  • Steroid usage
  • Continued pressure
  • Poor nutrition
  • Cytotoxic substances
  • Malignancies

31
  • Factors Affecting Normal Wound Healing
  • Foreign bodies
  • Cigarette smoking
  • Radiation
  • Alcoholism
  • Aging
  • Compliance

32
  • 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

33
  • 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

34
Infection
35
  • Venous hypertension
  • superficial venous insufficiency
  • incompetent perforator vein with normal deep
    vein
  • venous hypertensioncapillary 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

36
Venous Stasis
37
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38
  • 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

39
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40
CHARCOT ARTHROPATHY
41
  • 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

42
  • 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

43
  • 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.

44
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45
  • 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

46
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47
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48
  • Foreign Bodies
  • Nidus for infection Hematomas, Dysvascularized
    bone, tendon, cartilage, metal objects, glass,
    wood, thorns

49
  • Smoking
  • Limits functional tissue perfusion
  • Cutaneous vasoconstriction and decreased wound
    contraction as a direct effect of nicotine

HIPAA
50
  • 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

51
Osteoradionecrosis
52
  • 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

53
CalciphylaxisPyoderma gangrenosum
  • Be aware!

54
Compliance
55
  • 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

56
Darco wedge Shoe
57
Reverse IPOS
58
Total Contact Cast
59
Total Contact Cast Holiday Version
60
Total Contact Cast Sports Version
61
Diabetic Shoes
62
Wheelchair
63
Canes, crutches, walkers
64
Roll a Bout
65
PRAFO Splint
66
  • Description
  • 15 gram tube
  • Contains 100 mg/g rhPDGF-BB (0.01)
  • Store at 36-46F / 2-8C (refrigeration)

trademark
67
ORC/Collagen(Promogran Matrix Wound Dressing)
45 Oxidized Regenerated Cellulose / 55
Collagen A bioresorbable, amorphous,
open-pored matrix
Source Angiogenesis Clinic, Boston
Reference Cullen B, Smith R, McCullochE, Silcock
D, Morrison L. Mechanism of action of PROMOGRAN,
a protease modulating matrix, for the treatment
of diabetic foot ulcers. Wound Rep Reg
20021016-25. Ovington L, Cullen B. Matrix
metalloprotease modulation and growth factor
protection. Podiatry Today 2002 Oct(Suppl)
2-13.
Trademark
68
PRISMA Matrix Components
69
  • Adjunct Therapies in Wound Healing
  • Apligraf Indicated for venous stasis ulcers.
    It is a bilayered, living skin construct which
    can be used in place of a split thickness skin
    graft. Histologically, it is very similar to
    human skin and has a functional epidermis and
    dermis.

70
APLIGRAF (Graftskin) APPROXIMATES SKIN IN
STRUCTURE AND BARRIER FUNCTION
71
HISTOLOGIC COMPARISON
APLIGRAF (Graftskin)
Human Skin
Photomicrographs of hematoxylin-eosine-stained
cross-sections of APLIGRAF (left) and human skin
(right) ?250.
72
Hyperbaric Oxygen Therapy (HBO)
73
  • Effects of HBO
  • Enhances collagen production
  • Enhances capillary angiogenesis
  • Increases oxygen tension in infected tissue and
    bone
  • Increases effect of neutrophils
  • Direct lethal effect on strict anaerobes
  • Inhibits production of exotoxins
  • Augments antibiotic effectiveness

74
  • HBO Indications
  • Clostridial Myonecrosis (gas gangrene)
  • Osteomyelitis
  • Necrotizing soft tissue infections
  • Non operable patient with arterial disease
    (TCPO2 studies)
  • Osteoradionecrosis
  • Necrotizing insect bites (Brown Recluse spider)
  • Diabetic foot wounds Wagner Grade 3 or more

75
  • Topical enzymatic debridement agents i.e.
    Accuzyme, Panafil, Santyl, Gladase
  • Topical antibiotics Silvadene, Iodosorb,
    bacitracin, Bactroban, Neosporin
  • Dressings gauze, hydrogels, alginates, foams
  • Dermagraft
  • Graftjacket
  • Anodyne
  • The VAC (Vacuum Assisted Closure)
  • Integra (dermal equivalent)

76
Integra
77
Healed
78
Dog Bite
79
Debridement and Skin Graft
80
Healed
81
Bad Dog!
82
Wound Care Centers
  • Hospital based facilities
  • Podiatry, Plastic Surgeons, Vascular Surgeons,
    General Surgeons, etc.
  • Specialty trained nurses in wound care
  • Latest treatment modalities
  • Hyperbaric oxygen chambers
  • Last resort?
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