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aaaabbbb > 2 - Principles of Wound Healing > Flashcards

2 - Principles of Wound Healing Flashcards

1
Q

Wound healing

A
  • Incision by a blade, trauma from a bullet and tissue death from a myocardial infarction all undergo a similar and predictable reparative process
  • Understanding how the body repairs damaged tissue is vital to treating and preventing wounds
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2
Q

Phases of wound healing from the “wound module”

A
  • Injury (not always included)
  • Inflammatory phase
  • Proliferative phase
  • Maturation
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3
Q

Mechanisms of wound repair

A

o Connective tissue deposition
o Epithelization
o Contraction

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4
Q

Types of woundn closure

A

o Primary intention
o Secondary intention
o Delayed primary closure
o Partial thickness (scratch or superficial abrasion)

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5
Q

Inflammatory phase

A
  • Characterized by hemostasis and inflammation
  • Collagen exposure during wound deformation activates the clotting cascade –> IMPORTANT
    o Damaged cells release thromboxane A2 and prostaglandin 2-alpha (vasoconstrictors)
    o Initial response limits the hemorrhage
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6
Q

Capillary vasodilation of the inflammatory phase

A
  • Capillary vasodilatation occurs as well in response to histamine release
    o This causes inflammatory cells to migrate to the wound bed
    o Vasodilation occurs to counteract the vasoconstriction –> “checks and balances”
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7
Q

1st and 2nd cells to show up during inflammatory phase

A
  • Platelets are “first response cells” and neutrophils are “second response cells”
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8
Q

Platelets during the inflammatory phase - 3 things they release

A

1st = Platelets (first response cell) release 3 things:
o Epidermal growth factors (EGF) –> regulates cell growth, proliferation, differentiation
o Platelet Derived Growth Factors(PDGF) –> regulates cell growth, blood vessels division
o Histamine

* During the inflammatory phase, the wound is stabilized through clot formation*

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9
Q

Neutrophils during inflammatory phse

A

Neutrophils (second response cell) migrate to the wound for complement mediated opsonization of bacteria (“packaging and getting rid of bacteria”)
o Vessel adherence (pavementing, margination)
o Diapedesis (movement through vessel walls)
o Chemotaxis (chemical directive to injury site)
o Phagocytosis (opsonization)

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10
Q

Macrophages during inflammatory phase

A

Macrophages are most essential cell for wound healing
o Initially you need neutrophils to “clean up,” but eventually you need macrophages to start initiating wound healing and regrowth of tissue
o Macrophages release Tumor Necrosis Factor (TNF) which stimulates fibroblasts (collagen) and angiogenesis

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11
Q

Other events promoting healing and new growth during inflammatory phase

A

o Transforming Growth Factor (TGF) will be present, which stimulates keratinocytes
o Increased blood flow and congestion is evident by the increased number of red cells
o The increase in neutrophils (dark segmented cells) is also evident as well as the increased protein exudates (pink substance)

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12
Q

3 stages of proliferative phase of wound healing

NEED TO KNOW

A

o **Epithelization
o **Angiogenesis
o ***Collagen deposition (granulation tissue formation)

Note that there is some overlap between these stages

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13
Q

Epithelialzation

A

Stage 1 of proliferative phase
o If basement membrane is intact, cells will migrate in a normal pattern (Example: 1st degree skin burn) - Normal layers of epidermis will be restored in 2-3 days
o If basement membrane destroyed, wound is re-epithelialized from cells in the periphery (Example: 2nd or 3rd degree burns)

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14
Q

Angiogenesis

A

Stage 2 of proliferative phase
o Stimulated by TNF-alpha
o Endothelial cell migration and capillary formation
o Maintains the granular bed
o Migration of capillaries (new capillary formation) delivers nutrients to the wound bed

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15
Q

Collagen deposition (granulation tissue formation)

A

Stage 3 of proliferative phase

Fibroblasts differentiate and lay down collagen fibers in varying patterns

  • Organized collagen = STRONG, disorganized, random collagen = WEAK
  • Collagen is much thicker during proliferative phase, thinner during maturation

Cytokines involved: IGF (insulin like growth factor), PDGF

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16
Q

Maturation phase

A
  • Begins 1-2 weeks after injury
  • Increased collagen and vascularity occur, wound contraction begins
  • At the beginning of the maturation phase the tensile strength of the skin is 30% of normal skin
    o Wound will not reach maximum strength until one year
  • Increased collagen deposition, increased blood flow, new capillaries
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17
Q

Graph on phases of wound healing

A
  • Here you can see the three phases (inflammation,
    proliferation, maturation)
  • Note the specific cells that are present during each
    phase and the significant overlap that is present
  • Oxygen availability is important here –> during the
    inflammatory phase, there really is no oxygen available,
    but as we progress through maturation, oxygen becomes
    available due to extensive angiogenesis
18
Q

Tensile strength graph

A
  • This graph shows the types of cells present in each
    phase as well, but in this graph focus on the tensile
    strength in each of the phases
  • Tensile strength continuously increases following injury
  • During fibroblastic phase there is a jump in strength that
    continues through maturation
  • At day 21 (beginning of maturation phase), the tensile
    strength is only at about 30%
19
Q

Collagen deposition graph

A
  • Same thing for tensile strength – from 0-21 days, you
    reach about 30% of normal tissue strength
  • Note that the collagen is deposited in a random
    orientation from 0-21 days, leading to significantly
    thicker collagen
  • This collagen then gets reorganized during the
    maturation phase and it becomes thinner
  • Don’t need to know specific dates, but know the
    ballpark time periods for these events
20
Q

LOCAL factors that affect wound healing

A
  • Blood Supply
  • Denervation
  • Hematoma (collection of blood)
  • Seroma (collection of serous fluid)
  • Infection
  • Mechanical Stress
  • Surgical Technique
  • Irrigation
  • Dressing materials
21
Q

GENERAL factors that affect wound healing

A
  • Age
  • Anemia
  • Anti-inflammatory drugs (controversial)
  • Corticosteroids
  • Malnutrition
  • Diabetes
  • Vitamin deficiency
22
Q

Wound healing principles

A

Things you need to address

  • Vascular perfusion
  • Bacterial balance
  • Nutritional balance
  • Control contributing factors (anything that contributed to trauma or breakdown)
23
Q

wound dehiscene

A

o Surgical site opens up and there is parting of the layers of the surgical wound

24
Q

Cause of wound dehiscence

A

o Infection, hematoma, seroma, poor surgical technique, inappropriate closure technique, excessive motion at the surgical site, patient non-compliance

25
Q

Primary intention

A

o Side to side closure of the wound with sutures

o Reapproximation of skin edges

26
Q

Considerations for primary intention

A

o Sutures can be placed under ideal circumstances
o Need to prep the skin
o Incision in the line of election for elective wounds
o Dermis has tensile strength, but tensile strength is not regained for several weeks
o Inflammation causes scarring
o Place epidermal sutures superficial

27
Q

Secondary intention

A
  • Wound is left open to granulate to closure
28
Q

Delayed primary closure

A
  • Wound is left open for a period of time and then primarily closed
  • Typically done when you have contamination/infection at the site
29
Q

Wound repair and closure

A
  • These are the RELATIVE contribution of the three principle mechanisms of wound healing in the different types of wounds
30
Q

Epithelialization

A
  • You have a breakdown of the superficial skin, but no penetration through basement membrane
  • Following debridement of the area, you see healthy granular base which will eventually heal on its own with NO SCAR since there was no damage to the basement membrane or dermis
  • The difference between epithelization and secondary intention is that the basement membrane has NOT been breached in epithelization and it HAS been breached in secondary intention
  • Note that since secondary intention involves a breach in basement membrane, a scar WILL form
31
Q

Chart on healing process for primary, secondary and partial thickness wound healing

A
  • Sutured = primary intention
  • Open = secondary intention
  • Partial thickness = epithelialization

Each of these will be assessed in terms of contraction, epithelialization and connective tissue deposition

32
Q

Sutured (primary intention)

A
  • No contraction
  • Slight epithelialization
  • High connective tissue deposition
33
Q

Open (secondary intention)

A
  • High contraction
  • Slight epithelialization
  • Moderate connective tissue deposition
34
Q

Partial thickness (epithelialization)

A
  • NO Contraction
  • HIGH epithelialization
  • NO connective tissue deposition

NOTE - the ONLY wound healing mechanism in play during partial thickness epitheliazatoin is the epithelialization itself ***

35
Q

Keloid

A

o Abnormal scar that extends beyond the boundary of the original skin injury
o Raised, thickened growth associated with pruritus and pain - pathophysiology unknown

36
Q

Histology of a keloid

A

o Scanning electron microscopy reveals randomly organized collagen fibers in a dense connective tissue matrix

37
Q

Location of keloids

A

o Sternum, deltoid area, upper back have increased susceptibility because these areas have elevated levels of muscle and skin tension
o Earlobes and posterior portion of the neck are also common place

38
Q

Trends in keloids

A

o More common in African American, Hispanics, Asians (as high as 16%)
o Familial predisposition is also noted -> Ask patient about history and family history

39
Q

Treatment for keloid

A

o 50% recurrence rate

o Compressive dressings, intralesional corticosteroid injections, cryosurgery, laser ablation

40
Q

Hypertrophic scars

A

o Defined as a widened or unsightly scar that does not extend beyond the original boundaries of the wound

Different from keloid with DOES extend beyond initial scar boundary

41
Q

Trends in hypertrophic scars

A

o Usually reach a certain size and then stabilizes or begins to regress
o No racial or familial preponderance noted

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