The Principles of Wound Healing

Report
Craig A. Blum, MD Fellow
Division of Plastic Surgery
Department of Surgery
Tulane University School of Medicine
Breast Reconstruction?
Free Tissue Transfer?
Digit Replants?
Facelifts?
Wounds.
Disclaimer
Game Plan
 Wound Basics
 Test Questions – Shelf, ABSITE
 Practical info – Taking care of wounds
 Short and Sweet
History of Wound Healing
 1700 BC Papyrus: Lint/animal grease/honey
 100 BC Egypt: Wound closure preserved soul
 1000 AD Gun Powder
 1500 AD Hot Oil
 20th Century Scientific Method
Wounds are serious business
Wounds
 Customize treatment
 No two patients OR
wounds are identical
58y DM, Neuropathy: unaware
of R foot gangrene
 Cause
 Condition of
patient
 Definitive
management?
Wounds
 Crush injury
wound
 Viability of
the remaining
tissues
 Ability to
salvage the
extremity
 Functionality
of the limb if
it can be
salvaged
Wounds
 Reconstructive
Ladder
 Simple to Complex
Formal Debridement, Elevation/ABI’s
Appropriate IV ABX, Wound Vac, Skin Graft
Review of Wound Healing
 Three basic types of healing
 Primary
 Delayed Primary
 Secondary
Primary
 Wound surfaces opposed
 Results optimal
 Clean wounds
Delayed Primary
 Left open initially
 Edges approximated 4-6 days later
 Less common
Secondary
 Surfaces not approximated
 Defect filled by granulation
 Covered with epithelium
 Dirty Wounds
 No Steri Strips
Secondary Wound Healing
Secondary Wound Healing
Secondary Wound Healing
Three Phases of Wound Healing
Inflammatory Phase
 Proliferative Phase
 Remodeling Phase

Inflammatory Phase
 Hemostasis and Inflammation
 24-48 hours
 Platelets  thrombus, chemotaxis
 NEUTROPHILS and MACROPHAGES
 Debride
 Growth factors
Inflammatory: Neutrophils
 Attracted by inflammatory mediators
 Oxygen-derived free radicals
 Debride wound
Inflammatory: Macrophages
 Debride (phagocytosis)
 Proinflammatory cytokines
 IL -1 (fever)
 Growth factors (TGF-B) attracts FIBROBLASTS
 NO (vasodilation)
Inflammatory Phase
Inflammatory Phase
Inflammatory Phase
Three Phases of Wound Healing
 Inflammatory Phase
 Proliferative Phase
 Remodeling Phase
Proliferative Phase
 Epithelization, Angiogenesis and Provisional
Matrix Formation
 Begins when wound is covered by epithelium
 48 h to 2-3 weeks
 Production of collagen is hallmark
 STRUCTURE
 FIBROBLASTS
Epithelialization
Basal epithelial cells
at the wound margin
flatten (mobilize)
and migrate into the
open wound
 Basal cells at margin
multiply (mitosis) in
horizontal direction
 Basal cells behind
margin undergo
vertical growth
(differentiation)

Proliferative: Fibroblast
 Work horse of wound repair
 Produce Granulation
Tissue:
well vascularized collagen,
supporting cells
Wound Contraction
 Actual contraction with pulling of edges
toward center making wounds smaller
 Myofibroblast: contractile properties
 (Secondary intention)
Epithelialization/Contraction
Epithelialization
Vaso C Vaso D (NO)
Inflammation, Prolif, Remodeling
Collagen Homeostasis
 After Wounding (Optimal Healing)
 48 hours +
Collagen production begins
 Synthesis with a net GAIN of collagen
 Initial increase in tensile strength due to
increased amount of collagen
 2-3 weeks to 2 years
 Remodeling with No net collagen gain

Collagen
 Fibroblast make type III collagen (Baby collagen)
 Replaced by type I (mature)
 Type 4 basement membrane
 Normal Skin
 collagen ratio 4 : 1 Type I/III
 Hypertrophic Scar
 collagen ratio 2 : 1 Type I/III
Three Phases of Wound Healing
 Inflammatory Phase
 Proliferative Phase
 Remodeling Phase
Maturation Phase
 Random to organized
fibrils
 Type III replaced by type I
 Wound may increase in
strength for up to 2 years
after injury
 Collagen organization
 Cross linking of
collagen
Maturation Phase
Sits up after hernia repair?
 Wound strength
increases slowly for 2
weeks
 Rapidly for 4 weeks
 By 6 weeks wound has
gained 50% of its
ultimate strength (80%
is as good as it gets)
Impaired Wound Healing
 FISTULA
 FRIENDS
 FB
 Radiation
 Infection
 Epith
 Nutrition
 DM, distal obst
Wound Healing
 To treat the wound, you have to treat the
patient
 Optimize the patient
 Circulatory
 Pulmonary
 Nutrition
 Associated diseases or conditions
 Oxygen
 Fibroblasts are oxygen-sensitive
 PO2 < 40 mmHg collagen synthesis cannot
take place
 Decreased PO2: most common cause of
wound infection
 Healing is Energy Dependent
 Proliferative Phase has greatly increased
metabolism and protein synthesis
 Edema
 Increased tissue pressure
 Compromise perfusion
 Cell death and tissue ulceration
 Infection
 Decreased tissue PO2 and prolongs the
inflammatory phase
 Impaired angiogenesis and epithelialization
 Increased collagenase activity
 Nutrition
 Low protein levels prolong inflammatory
phase
 Impaired fibroplasia
 Hydration
 A well hydrated wound will epithelialize
faster than a dry one
 Occlusive wound dressings hasten epithelial
repair and control the proliferation of
granulation tissue
 Temperature
 Wound healing is accelerated at
environmental temperatures of 30°C
 Tensile strength decreases by 20% in a cold
(12°C) wound environment
 Denervation
 Denervation has no effect on either wound
contraction or epithelialization
 Diabetes Mellitus
 Larger arteries, rather than the
arterioles, are typically affected
 Impaired oxygen and nutrient delivery
 Affinity of glycosylated hemoglobin for
oxygen contributing to low O2 delivery
 Impaired phagocytosis and bacterial
killing
 Neuropathy
 Radiation Therapy
 Acute radiation injury





stasis and occlusion of small vessels
fibrosis and necrosis of capillaries
direct, permanent, adverse effect on fibroblast
may be progressive
fibroblast defects are the central problem in
the healing of chronic radiation injury
 Medications
 Steroids





Stabilize lysosomes and arrest of inflammation
response
Inhibit both macrophages and neutrophils
Interferes with fibrogenesis, angiogenesis, and
wound contraction
Also direct effect on Fibroblasts
 Minimal endoplasmic reticulum
Vitamin A
 oral ingestion of 25,000 IU per day pre op and 3d
post op (not to pregnant women)
 Restores inflammatory response and promotes
epithelializaton
 Does not reverse detrimental effects on contraction
and infection
 Nutritional Supplements
 Vitamin C ( Ascorbic Acid)


Essential cofactor in synthesis of
collagen
Excessive concentrations of ascorbic acid
do not promote supranormal healing
 Vitamin E



Therapeutic efficacy and indications
remain to be defined
Large doses of vitamin E inhibit healing
Increase the breaking strength of wounds
exposed to preoperative irradiation
 Nutritional Supplements
 Glutamine (small bowel)
Enhance actions of lymphocytes, macrophages and
neutrophils
 Glycine
 Inhibitory effect on leukocytes, might reduce
inflammation related tissue injury
 Zinc
 common constituent of dozens of enzymes
 Influences B and T cell activity
 epithelial and fibroblastic proliferation is impaired
in patients with low serum zinc levels

Factors in Wound Healing
 Smoking
 1ppd = 3x ↑ freq of flap necrosis
 2ppd = 6x ↑ freq of flap necrosis
 Nicotine acts via the sympathetic system (PATCHES)
Vasoconstriction and limit distal perfusion
 1 cigarette = vasoconstriction > 90 min
 Decrease proliferation of erythrocytes, macrophages and
fibroblasts
 Smoke contains high levels of carbon monoxide
 shifts the oxygen-hemoglobin curve to the left
 decreased tissue oxygen delivery

Syndromes Associated with Abnormal
Wound Healing
 Cutis Laxa
 Characterized by degenerative changes in the elastic
fibers resulting in loose, pendulous skin
 Ehlers-Danlos Syndrome
 Think defective collagen metabolism
 AD and recessive patters
 10 phenotypes
Syndromes Associated with
Abnormal Wound Healing
 Ehlers-Danlos Syndrome
 Four major clinical features




Skin hyper-extensibility
Joint hyper-mobility
Tissue fragility
Poor wound healing
Electrostimulation
 Electrical current applied to wounds
 Increases migration of cells
 109% increase in collagen
 40% increase in tensile strength
 1 to 50 mA direct or pulsed based on wound
Hyperbaric Oxygen
 Developed 1662 by Henshaw: Domicillium
 Atmospheric pressure at sea level = 1 ATA = 1.5ml
O2/dL
 Normal SubQ O2 tension is 30-50 mmHg.
 SubQ O2 tension < 30 mmHg = chronic wound
Excessive Healing
 Hypertrophic Scars
 Keloids
Hypertropic Scar
Keloids
 Extends beyond original bounds
 Raised and firm
 Rarely occur distal to wrist or knee
 Predilection for sternum, mandible and deltoid
 Rate of collagen synthesis increased
 Water content higher
 Increased glycosaminoglycans
Keloid Treatment
 Triamcinolone (steroid) injections
 3-4 weeks
 Cross linking modulated
 Injections continued until no excess abnormal
collagen
 Excise
 Prevention during healing – pressure and injection
Keloid
Keloid
Keloid Scar
Keloid Scar
Marjolin’s Ulcer
 Jean-Nicolas Marjolin (1828)
 Aggressive ulcerating SCC
 Occurs in setting of chronic
inflammation
 Burn wounds
 Venous stasis ulcers
 Previous radiation therapy
 Characterized by
 Slow growth
 Painless
 Persistent granulation
Questions
 The proliferative phase of wound healing occurs
how long after the injury?
1 day
B. 2 days
C. 7 days
D. 14 days
A.
 The proliferative phase of wound healing occurs
how long after the injury?
1 day
B. 2 days
C. 7 days
D. 14 days
A.
 Which type of collagen is most important in wound
healing?
Type III
B. Type V
C. Type VII
D. Type XI
A.
 Which type of collagen is most important in wound
healing?
Type III
B. Type V
C. Type VII
D. Type XI
A.
 The tensile strength of a wound reaches normal
(pre-injury) levels:
10 days after injury
B. 3 months after injury
C. 1 year after injury
D. never
A.
 The tensile strength of a wound reaches normal
(pre-injury) levels:
10 days after injury
B. 3 months after injury
C. 1 year after injury
D. never
A.
 Steroids impair wound healing by:
Decreasing angiogenesis and macrophage
migration
B. Decreasing platelet plug integrity
C. Increasing release of lysosomal enzymes
D. Increasing fibrinolysis
A.
 Steroids impair wound healing by:
Decreasing angiogenesis and macrophage
migration
B. Decreasing platelet plug integrity
C. Increasing release of lysosomal enzymes
D. Increasing fibrinolysis
A.
 Supplementation of which of the following
micronutrients improves wound healing in patients
without micronutrient deficiency?
A. Vitamin C
B. Vitamin A
C. Selenium
D. Zinc
 Supplementation of which of the following
micronutrients improves wound healing in patients
without micronutrient deficiency?
A. Vitamin C
B. Vitamin A
C. Selenium
D. Zinc
 Signs of malignant transformation in a chronic
wound include:
Persistent granulation tissue with bleeding
B. Overturned wound edges
C. Non-healing after 2 weeks of therapy
D. Distal edema
A.
 Signs of malignant transformation in a chronic
wound include:
Persistent granulation tissue with bleeding
B. Overturned wound edges
C. Non-healing after 2 weeks of therapy
D. Distal edema
A.
 The treatment of choice for keloids is:
Excision alone
B. Excision with adjuvant therapy (e.g. radiation)
C. Pressure treatment
D. Intralesional injection of steroids
A.
 The treatment of choice for keloids is:
Excision alone
B. Excision with adjuvant therapy (e.g. radiation)
C. Pressure treatment
D. Intralesional injection of steroids
A.
 The major cause of impaired wound healing is:
Anemia
B. Diabetes mellitus
C. Local tissue infection
D. Malnutrition
A.
 The major cause of impaired wound healing is:
Anemia
B. Diabetes mellitus
C. Local tissue infection
D. Malnutrition
A.
 Bradykinin, serotonin, and histamine in wounds
are released from:
Lymphocytes
B. Mast cells
C. Polymorphonuclear leukocytes
D. Platelets
A.
 Bradykinin, serotonin, and histamine in wounds
are released from:
Lymphocytes
B. Mast cells
C. Polymorphonuclear leukocytes
D. Platelets
A.
 Platelets in the wound form a hemostatic clot and
release clotting factors to produce:
Fibrin
B. Fibrinogen
C. Thrombin
D. Thromboplastin
A.
 Platelets in the wound form a hemostatic clot and
release clotting factors to produce:
Fibrin
B. Fibrinogen
C. Thrombin
D. Thromboplastin
A.
 In a healing wound, metalloproteinases are
responsible for:
Establishing collagen cross-link
B. Glycosylation of collagen molecules
C. Incorporation of hydroxyproline into the collagen chain
D. Initiating collagen degradation
A.
 All of the following statements about keloids are true
except?
Keloids do not regress spontaneously
B. Keloids extend beyond the boundaries of the original
wound
C. Keloids or hypertrophic scars are best managed by excision
and careful reapproximation of the wound
D. Keloid tissue contains an abnormally large amount of
collagen.
A.
 All of the following statements about keloids are true
except?
Keloids do not regress spontaneously
B. Keloids extend beyond the boundaries of the original
wound
C. Keloids or hypertrophic scars are best managed by
excision and careful reapproximation of the wound
D. Keloid tissue contains an abnormally large amount of
collagen.
A.
 The following photograph most
accurately demonstrates:
Hypertropic Scar
B. Auricular Lymphedema
C. Keloid Scar
D. “Cauliflower” ear
A.
 The following photograph most
accurately demonstrates:
Hypertropic Scar
B. Auricular Lymphedema
C. Keloid Scar
D. “Cauliflower” ear
A.
 The Proliferative Phase of wound healing is classically
described as beginning:
A. Immediately after injury
B. When the wound is covered with epithelium
C. When the collagen content has reached equilibrium
D. When the macrophage enters the wound
 The Proliferate Phase of wound healing is classically
described as beginning:
A. Immediately after injury
B. When the wound is covered with epithelium
C. When the collagen content has reached equilibrium
D. When the macrophage enters the wound
 Under ideal circumstances the tensile strength of the
wounded area reaches what % of strength compared to
normal skin?
10-20%
B. 20-40%
C. 60-70%
D. 70-90%
A.
 Under ideal circumstances the tensile strength of the
wounded area reaches what % of strength compared to
normal skin?
10-20%
B. 20-40%
C. 60-70%
D. 70-90%
A.
 Which of the following does NOT affect wound
healing
A. Infection
B. Hydration
C. Nutrition
D. Denervation
 Which of the following does NOT affect wound
healing
A. Infection
B. Hydration
C. Nutrition
D. Denervation
Final Thoughts
 Wet to dry dressings
 VAC
 Wound care nurses
 Look at wounds
 Staples and running sutures
 Abscesses
 Thank You

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