Principles of Wound Healing

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Principles of Wound Healing
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WHAT IS A WOUND?
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Wound(woond) Break in the continuity of soft or
hard parts of the body structures caused by
violence or trauma to tissues.
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Common chronic wounds of the skin and soft
tissues Arterial Venous Pressure Diabetes Collagen
Vascular disease Udder
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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.
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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.
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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.
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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.

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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.

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Good Wound CareClinical practices which
support the normal healing process
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Key Considerations Good Wound Care

• Infection control
• Sharp Debridement
• Moist wound environment
• Off-loading/compression therapy
• Nutritional status

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Sharp Debridement

• Removes
• Devitalized tissues
• Bacteria and proteolytic enzymes
• Senescent cells

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

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

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• 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

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• 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

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• 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

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

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

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

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• 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

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• 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

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Infection
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• 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

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Venous Stasis
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• 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

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CHARCOT ARTHROPATHY
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• 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

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• 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

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• 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.

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• 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

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

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

HIPAA
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• 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

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Osteoradionecrosis
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• 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

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CalciphylaxisPyoderma gangrenosum

• Be aware!

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Compliance
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• 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

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

trademark
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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
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PRISMA Matrix Components
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• 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.

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APLIGRAF (Graftskin) APPROXIMATES SKIN IN
STRUCTURE AND BARRIER FUNCTION
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HISTOLOGIC COMPARISON
APLIGRAF (Graftskin)
Human Skin
Photomicrographs of hematoxylin-eosine-stained
cross-sections of APLIGRAF (left) and human skin
(right) ?250.
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Hyperbaric Oxygen Therapy (HBO)
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• 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

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• 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

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• 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)

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Integra
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Healed
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Dog Bite
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Debridement and Skin Graft
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Healed
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Bad Dog!
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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?